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Postgraduate Medical Journal Dec 1987Autonomic nervous system integrity has been assessed in 30 alcoholic subjects and 30 age-sex matched controls using five simple tests of cardiovascular responses. There...
Autonomic nervous system integrity has been assessed in 30 alcoholic subjects and 30 age-sex matched controls using five simple tests of cardiovascular responses. There was evidence of parasympathetic neuropathy alone in five of the alcoholic subjects (16%) and of combined parasympathetic and sympathetic neuropathy in an additional six (20%). None of the controls showed any abnormality. Within the alcoholic group, those with autonomic neuropathy were older, were more likely to be female and to have established alcoholic liver disease. Symptoms were a poor guide to the presence or absence of autonomic neuropathy.
Topics: Adult; Aged; Alcoholism; Autonomic Nervous System Diseases; Female; Hemodynamics; Humans; Male; Middle Aged
PubMed: 3451229
DOI: 10.1136/pgmj.63.746.1033 -
Annals of Neurology Jul 2011While inflammatory pain is well described in skeletal muscle, neuropathic muscle pain remains to be clarified. We used 3 well-established rodent models of peripheral... (Comparative Study)
Comparative Study
OBJECTIVE
While inflammatory pain is well described in skeletal muscle, neuropathic muscle pain remains to be clarified. We used 3 well-established rodent models of peripheral neuropathy to evaluate for muscle pain.
METHODS
In rats exposed to either of 2 neurotoxic cancer chemotherapies, paclitaxel or oxaliplatin, or to alcohol consumption, we assessed the evolution of mechanical hyperalgesia in skeletal muscle and skin, in the same animal. To explore the involvement of protein kinase C epsilon (PKCε), a second messenger implicated in some forms of neuropathic pain, antisense oligodeoxynucleotides (AS-ODNs) or mismatch ODNs (MM-ODNs) for PKCε were administered intrathecally.
RESULTS
Rats submitted to models of chemotherapy-induced and alcohol-induced neuropathy developed persistent muscle hyperalgesia, which evolved in parallel in muscle and skin. The administration of PKCε AS, which has been shown to mediate cutaneous hyperalgesia in paclitaxel and ethanol models of neuropathic pain, also inhibited muscle hyperalgesia induced by these agents. Stopping AS-ODN was associated with the reappearance of hyperalgesia at both sites. The AS-ODN to PKCε treatment was devoid of effect in both muscle and skin in the oxaliplatin neuropathy model.
INTERPRETATION
Our results support the suggestion that neuropathic muscle pain may be a greater clinical problem than generally appreciated.
Topics: Alcohol Drinking; Alcoholic Neuropathy; Animals; Antineoplastic Agents; Disease Models, Animal; Male; Muscle, Skeletal; Pain; Pain Measurement; Peripheral Nervous System Diseases; Rats; Rats, Sprague-Dawley
PubMed: 21786301
DOI: 10.1002/ana.22382 -
Case Reports in Ophthalmology 2023A 56-year-old man with a medical history of alcoholic cirrhosis presented with acute bilateral loss of vision. On admission, the patient had pale skin and low arterial...
A 56-year-old man with a medical history of alcoholic cirrhosis presented with acute bilateral loss of vision. On admission, the patient had pale skin and low arterial pressure. Ophthalmic examination demonstrated a visual acuity of 6/9 in the right eye and the absence of light perception in the left. Automated perimetry revealed a superior altitudinal defect in the right eye. Optic disc swelling, flame-shaped hemorrhages, and several cotton-wool spots were evident in both eyes on fundoscopy. Lab results confirmed severe anemia. Following prompt correction of the anemia, the altitudinal defect remained unchanged. However, visual acuity in the right eye improved significantly in a few days. The potential association of anemia with both papilledema and non-arteritic anterior ischemic optic neuropathy (NA-AION) is discussed, with a focus on possible pathophysiological mechanisms. The necessity for routine anemia screening, encompassing complete blood count, serum iron, and vitamin B12 levels, and subsequent rapid correction in these patients, is emphasized.
PubMed: 37901626
DOI: 10.1159/000531999 -
Postgraduate Medical Journal Jul 2003Autonomic neuropathy has been reported in patients with alcoholic liver disease but information on its occurrence in patients with non-alcoholic liver disease is...
BACKGROUND
Autonomic neuropathy has been reported in patients with alcoholic liver disease but information on its occurrence in patients with non-alcoholic liver disease is contradictory.
AIM
To assess autonomic functions in patients with alcoholic and non-alcoholic liver disease.
STUDY DESIGN
Autonomic function using five standard tests was examined in 20 cirrhotics (10 alcoholics and 10 non-alcoholics) and 20 age and sex matched controls. The extent of autonomic dysfunction was determined in the patients and a comparison between the characteristics of patients with and without autonomic neuropathy was made.
RESULTS
Sixteen (80%) of the cirrhotic subjects were found to have evidence of autonomic neuropathy. Of these, three (15%) patients had early parasympathetic damage, five (25%) had definite parasympathetic damage, and eight (40%) had combined (that is, both parasympathetic and sympathetic) damage. Nine (90%) of the alcoholics and seven (70%) of the non-alcoholics had autonomic dysfunction. Only one patient belonging to the alcoholic group had clinical evidence of peripheral neuropathy. Moreover, there was no significant association between subjective symptoms of autonomic neuropathy and objective evidence of autonomic damage as assessed by autonomic function tests. Autonomic dysfunction was significantly more frequent in advanced liver disease compared with early liver damage. Nine (75%) out of 12 cirrhotic subjects belonging to Child class B and six (85.7%) of the seven patients belonging to Child class C had autonomic neuropathy.
CONCLUSION
This study shows that autonomic neuropathy is common in cirrhotic subjects, that it is found with comparable frequency in alcoholics and non-alcoholics, and that it increases in severity with increase in extent of liver damage, suggesting that liver damage contributes to the neurological deficit.
Topics: Autonomic Nervous System Diseases; Blood Pressure; Case-Control Studies; Heart Rate; Humans; Liver Cirrhosis; Posture; Respiration
PubMed: 12897221
DOI: 10.1136/pmj.79.933.408 -
Liver Transplantation : Official... Dec 2004Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy,...
Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy, pancreatitis, central nervous system injury, and neuropathy) is widely regarded as an absolute contraindication to liver transplantation, despite a lack of data on the effect of transplantation on these complications. We describe such a patient who presented with decompensated alcoholic liver disease and moderately severe peripheral neuropathy. Both his liver failure and neuropathy progressed despite 9 months abstinence and intensive nutritional support. By 12 months post-transplant, however, this patient had regained almost normal muscle strength, with associated recovery in sensory and motor conduction velocities. Direct alcohol toxicity, nutritional and vitamin deficiencies, and liver failure were all likely etiologic factors in this patient's neuropathy. In conclusion, this case suggests that peripheral neuropathy in a patient with alcoholic cirrhosis may resolve following liver transplantation and should not constitute a contraindication to transplantation, even when it is disabling.
Topics: Alcoholic Neuropathy; Humans; Liver Cirrhosis, Alcoholic; Liver Transplantation; Male; Middle Aged; Motor Neurons; Muscle, Skeletal; Neural Conduction; Neurons, Afferent; Postoperative Period; Recovery of Function; Time Factors
PubMed: 15558589
DOI: 10.1002/lt.20282 -
Hepatology (Baltimore, Md.) Mar 1996Autonomic neuropathy (AN) is seen in both alcohol-induced and non-alcohol-induced liver disease, and when present is an independent predictor of mortality. We postulated...
Autonomic neuropathy (AN) is seen in both alcohol-induced and non-alcohol-induced liver disease, and when present is an independent predictor of mortality. We postulated that patients who were awaiting liver transplantation are likely to have a high prevalence of autonomic neuropathy with an associated increase in mortality. To test our hypothesis, we evaluated the presence of autonomic neuropathy using a battery of tests in 33 patients awaiting liver transplantation and prospectively followed them to determine their prognosis. Twenty-two of 33 (67%) patients with liver disease had evidence of autonomic neuropathy; of these, 12 (36%) had evidence of definite and 10 (31%) had early autonomic neuropathy. The prevalence of AN was similar in alcohol-induced and non-alcohol-induced liver disease. Using Child-Pugh classification, 14.3% Child A, 31.3% Child B, and 60% Child C had definite autonomic neuropathy. Six patients died during a median observation period of 10 months, and all had AN. Kaplan-Meier survival analysis showed a significantly higher mortality (P=.05) in patients with AN. On the basis of this observation, we suggest that consideration should be given for early liver transplantation in patients with advanced liver disease and autonomic neuropathy.
Topics: Adult; Aged; Autonomic Nervous System Diseases; Chi-Square Distribution; Cohort Studies; Female; Humans; Liver Diseases; Liver Diseases, Alcoholic; Liver Transplantation; Male; Middle Aged; Prevalence; Prognosis; Prospective Studies; Survival Rate
PubMed: 8617426
DOI: 10.1002/hep.510230311 -
Cancers Sep 2017Previously called Crow-Fukase syndrome, POEMS syndrome is characterized by poly-neuropathy, osteo-sclerotic myeloma, organomegaly, endocrinopathy, monoclonal plasma cell...
UNLABELLED
Previously called Crow-Fukase syndrome, POEMS syndrome is characterized by poly-neuropathy, osteo-sclerotic myeloma, organomegaly, endocrinopathy, monoclonal plasma cell disorder, and skin changes. Extremely elevated levels of serum vascular endothelial growth factor (VEGF) are characteristic of the syndrome. Chronic hepatitis B (HBV) and C (HCV) infections can also be present in POEMS. The pathogenesis of the syndrome is not well understood. The link between chronic alcohol consumption and this malignant condition has not been reported until now. In addition, no previous study has evaluated the influence of cytokine and chemokines or viruses in the severity and evolution of POEMS.
OBJECTIVES
(1) to describe a heavy-alcohol user, who was diagnosed with POEMS; (2) to demonstrate the utility of quantitative measurement of serum levels of VEGF in the diagnosis of POEMS and the monitoring of therapeutic interventions; (3) to demonstrate that overproduction of pro-inflammatory cytokines is a characteristic of POEMS.
METHODS
We describe a case of a POEMS patient presenting HCV and who is a heavy drinker; we compare the serum levels of cytokines and chemokines between the POEMS patient with 80 patients with HCV, 12 healthy controls, and 80 individuals with alcoholic liver disease (ALD). We quantified (ELISA pg/mL) the levels of VEGF, Interferon gamma (IFN-γ), Tumor Necrosis Factor alpha (TNF-α), Regulated-upon-Activation Normal-T-cell-Expressed and presumably-Secreted (RANTES), and Nuclear Factor kappa-B (NFκB).
RESULTS
In POEMS patients, VEGF levels were elevated versus control or other diseases, TNFα levels were higher versus control, but lower when compared with HCV or ALD patients. VEGF levels in POEMS patients decreased with therapeutic intervention.
CONCLUSIONS
Chronic alcohol misuse can be a strong risk factor to rare malignancies such as POEMS syndrome. Extreme elevation of VEGF levels is diagnostic for POEMS syndrome, and should be followed to assess response to therapy. In addition, other comorbidities should be considered individually to ensure personalized therapeutic intervention.
PubMed: 28946631
DOI: 10.3390/cancers9100129 -
BMC Ophthalmology Apr 2023In countries where alcoholic beverages are legally prohibited, methanol toxicity usually occurs due to ingesting homemade alcoholic drinks. The initial ophthalmologic...
INTRODUCTION
In countries where alcoholic beverages are legally prohibited, methanol toxicity usually occurs due to ingesting homemade alcoholic drinks. The initial ophthalmologic symptoms of methanol toxicity typically appear 6-48 h after ingestion, and the severity of symptoms varies widely from mild and painless decreased vision to no-light perception vision.
METHODS
This prospective study examines 20 patients with acute methanol poisoning within 10 days of use. Patients underwent ocular examinations, BCVA (Best Corrected Visual Acuity) recording, and OCTA (Optical Coherence Tomography Angiography) of the macula and optic disc. BCVA measurement and imaging were repeated one month and three months after intoxication.
RESULTS
There was a statistically significant reduction in superficial parafoveal vascular density (P-value = 0.026), inner retinal thickness (P-value = 0.022), RNFL (Retinal Nerve Fiber Layer) thickness (P-value = 0.031), and an increase in cup to disc ratio (P-value < 0.001), and central visual acuity (P-value = 0.002) in this time course. However, there was no statistically significant difference in FAZ (Foveal Avascular Zone) area (P-value = 0.309), FAZ perimeter (P-value = 0.504), FD-300 (Foveal density, vascular density within a 300 μm wide region of the FAZ) (P-value = 0.541), superficial vascular density (P-value = 0.187), deep foveal vascular density (P-value = 0.889), deep parafoveal vascular density (P-value = 0.830), choroidal flow area (P-value = 0.464), total retinal thickness (P-value = 0.597), outer retinal thickness (P-value = 0.067), optic disc whole image vascular density (P-value = 0.146), vascular density inside the disc (P-value = 0.864), or peripapillary vascular density (P-value = 0.680) at different times.
CONCLUSION
Over time, methanol poisoning can cause changes in retinal layers thickness, vasculature, and optic nerve head. The most important changes include cupping of the optic nerve head, reduction in RNFL thickness, and inner retinal thickness.
Topics: Humans; Methanol; Tomography, Optical Coherence; Prospective Studies; Retinal Vessels; Case-Control Studies; Angiography; Optic Nerve Diseases; Fluorescein Angiography
PubMed: 37098467
DOI: 10.1186/s12886-023-02937-x -
The Journal of Neuroscience : the... Oct 2010Analgesic efficacy varies depending on the pain syndrome being treated. One reason for this may be a differential effect of individual pain syndromes on the function of...
Analgesic efficacy varies depending on the pain syndrome being treated. One reason for this may be a differential effect of individual pain syndromes on the function of the endogenous pain control circuits at which these drugs act to produce analgesia. To test this hypothesis, we examined the effects of diverse (i.e., ongoing inflammatory, neuropathic, or chronic widespread) pain syndromes on analgesia induced by activation of an opioid-mediated, noxious stimulus-induced endogenous pain control circuit. This circuit was activated by subdermal capsaicin injection at a site remote from the site of nociceptive testing. Analgesia was not affected by carrageenan-induced inflammatory pain or the early phase of oxaliplatin neuropathy (a complication of cancer chemotherapy). However, the duration of analgesia was markedly shorter in the late phase of oxaliplatin neuropathy and in alcoholic neuropathy. A model of fibromyalgia syndrome produced by chronic unpredictable stress and proinflammatory cytokines also shortened analgesia duration, but so did the same stress alone. Therefore, since chronic pain can activate neuroendocrine stress axes, we tested whether they are involved in the attenuation of analgesic duration induced by these pain syndromes. Rats in which the sympathoadrenal axis was ablated by adrenal medullectomy showed normal duration pain-induced analgesia in groups with either late-phase oxaliplatin neuropathy, alcoholic neuropathy, or exposure to sound stress. These results support the suggestion that pain syndromes can modulate activity in endogenous pain control circuits and that this effect is sympathoadrenal dependent.
Topics: Analgesia; Analgesics; Analysis of Variance; Animals; Capsaicin; Male; Nerve Net; Pain; Rats; Rats, Sprague-Dawley
PubMed: 20943910
DOI: 10.1523/JNEUROSCI.2867-10.2010 -
Journal of Neurology, Neurosurgery, and... Feb 1971To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles,...
To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.
Topics: Adult; Aged; Alcoholism; Biopsy; Chronic Disease; Electromyography; Female; Histocytochemistry; Humans; Male; Middle Aged; Muscle Spindles; Muscular Atrophy; Neural Conduction; Neuromuscular Diseases
PubMed: 4251669
DOI: 10.1136/jnnp.34.1.86