Etiology Of Neuropathy Research Articles

What is associated with painful polyneuropathy? A cross-sectional analysis of symptoms and signs in patients with painful and painless polyneuropathy.

It is still unclear how and why some patients develop painful and others painless polyneuropathy. The aim of this study was to identify multiple factors associated with painful polyneuropathies (NeuP). A total of 1181 patients of the multicenter DOLORISK database with painful (probable or definite NeuP) or painless (unlikely NeuP) probable or confirmed neuropathy were investigated clinically, with questionnaires and quantitative sensory testing. Multivariate logistic regression including all variables (demographics, medical history, psychological symptoms, personality items, pain-related worrying, life-style factors, as well as results from clinical examination and quantitative sensory testing) and machine learning was used for the identification of predictors and final risk prediction of painful neuropathy. Multivariate logistic regression demonstrated that severity and idiopathic etiology of neuropathy, presence of chronic pain in family, Patient-Reported Outcomes Measurement Information System Fatigue and Depression T-Score, as well as Pain Catastrophizing Scale total score are the most important features associated with the presence of pain in neuropathy. Machine learning (random forest) identified the same variables. Multivariate logistic regression archived an accuracy above 78%, random forest of 76%; thus, almost 4 out of 5 subjects can be classified correctly. This multicenter analysis shows that pain-related worrying, emotional well-being, and clinical phenotype are factors associated with painful (vs painless) neuropathy. Results may help in the future to identify patients at risk of developing painful neuropathy and identify consequences of pain in longitudinal studies.

Just supplement Thiamine! A simple yet dramatic solution! (P9-4.004)

<h3>Objective:</h3> We present a case showing how while the diagnostic process in neuropathy may be long and cumbersome, the solution is usually simple, dramatic and life changing. <h3>Background:</h3> 55-year-old female with acute-on-chronic, rapidly progressive numbness and weakness. She first noted numbness and tingling in her feet over 8 years ago, but with rapid progression over the past year up to her trunk and hands. She presented to the ER after falling in the house, laying on the floor for hours, unable to be lifted by her husband. Examination revealed several bruises, symmetric wasting of upper and lower extremity muscles, proximal greater than distal weakness, loss of pinprick, vibration and temperature sensation from toes up to the thighs. She was areflexic with bowel and bladder incontinence and urine retention of 1L on arrival. She gave a history of excessive alcohol intake since her teenage years, with a heavy increase in intake over the COVID pandemic due to loss of employment and depression. Low folic acid, ESR 72, CT abdomen notable for steatohepatitis, fecal loading and urine retention. CSF analysis showed no albumino-cytological dissociation. Autoimmune workup, RPR, B12, serum copper, CSF paraneoplastic panel, CT chest, MRI brain and complete spine were unremarkable. EMG/NCV showed moderate, length dependent, sensory-motor axonal polyneuropathy. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> She was started on high dose thiamine and folic acid supplementation in hospital. Initially, she was unable to feed herself, turn in bed or sit without support. She slowly recovered, regained continence and can ambulate independently with a walker now. She can play the piano. <h3>Conclusions:</h3> Thiamine associated neuropathy or Dry Beri-Beri can present with axonal predominant sensorimotor polyneuropathy that can mimic Guillain Barre Syndrome. While workup for other etiologies of neuropathy should be simultaneously pursued in alcoholics, thiamine supplementation is a simple treatment that can lead to satisfying and dramatic results. <b>Disclosure:</b> Dr. Bhende has nothing to disclose. Dr. Zafar has nothing to disclose. Dr. Prabhu has nothing to disclose. Dr. Undavia has nothing to disclose.

Evaluation of altered patterns of tactile sensation in the diagnosis and monitoring of leprosy using the Semmes-Weinstein monofilaments.

Leprosy neuropathy is the most common peripheral neuropathy of infectious etiology worldwide; it is characterized as asymmetric and focal multiple mononeuropathy. Semmes-Weinstein monofilament (SWM) test is a simple method to assess sensory nerve function. In this prospective cohort study, a dermatologist carried out hands and feet tactile sensation test with SWM in 107 multibacillary leprosy patients at diagnosis and in 76 patients at the end of treatment from 2016 to 2019. At diagnosis, 81/107 (75.7%) patients had some degree of functional disability, and 46 (43%) of them had altered SWM-test in the hands and 94 (87.9%) of them in the feet. After one year of multibacillary multidrug therapy, the disability decreasing to 44/76 patients (57.9%) and decreasing of the percentual of patients with altered SWM-test to 18% for the hands, and to 28.7% for the feet. At the end of treatment, the number of SMW-test points presented improvement in the hands of 22 (28.9%) patients, and in the feet of 47 (61.8%). In the hands, by SWM-test, only the radial nerve point demonstrated a significant asymmetry, while in the feet, the difference between the sum of altered SWM-test points showed significant asymmetry between both sides, highlighting the tibial nerve for the establishment of asymmetric leprosy neuropathy. In Spearman's correlation analysis, a positive correlation with statistical significance was observed between the number of hands and feet SWM altered points at diagnosis and the degree of disability at diagnosis (0.69) and at the end of the treatment (0.80). The patterns of hands and feet tactile sensation at diagnosis and their consequent modifications with the anti-leprosy drugs define the bacterial etiology of neuropathy, an important tool for the clinical diagnosis and follow up of the disease, highlighting the tibial nerve findings, the most affected nerve among leprosy patients by SWM-test, with significant asymmetry and focality impairments.

The Case for Moxibustion for Painful Syndromes: History, principles and rationale.

Traditional Chinese Medicine (TCM) has evolved over thousands of years. TCM practitioners use various approaches (such as acupuncture and tai chi) as well as herbal products to address health problems. Though lesser known in the west, the practice of Moxibustion is an integral part of Traditional East Asian Medicine. Moxibustion is an important non-invasive treatment that has shown to be beneficial in treating painful syndromes including neuropathy. It has been suggested that moxibustion may alleviate neuroinflammation by inhibiting NF-kB and by activating Nrf2. These anti-inflammatory and protective mechanisms could be key to exploring the use of moxibustion in treating other etiologies of neuropathy including HIV. There is ample scope for future study in this area and consideration of the history, development and practical applications of moxibustion therapy may be of help in this regard. This article seeks to explore the background, principles, and application of moxibustion in the clinical setting with particular emphasis on its potential for symptom management in the treatment of neuropathy and pain.

Elevated Creatinine Kinase in Peripheral Neuropathy Is Associated With Muscle Cramping.

Introduction: Serum Creatinine Kinase (CK) is a non-specific marker of muscle damage. There has been limited investigation of the association between peripheral neuropathy and CK elevation (hyperCKemia).Methods: We performed a chart review to investigate the CK level in peripheral neuropathies. Demographics, clinical history, physical exam, electrodiagnostic data, CK level, statin use, etiology of neuropathy, and concomitant neuromuscular disorders were recorded. HyperCKemia was defined using our laboratory cutoff values of >180 U/L (women) and >220 U/L (men).Results: We identified 450 patients with peripheral neuropathy who had CK testing, 92 (20.4%) of whom had hyperCKemia. Sixty-one of those patients (13.5% of the total figure) had a concomitant etiology that could explain the CK elevation. Thirty-one patients (6.9%) had no other identifiable etiology for their hyperCKemia beyond the neuropathy. The average CK level in the latter cohort with hyperCKemia was 376 U/L (women: 312 U/L; men: 444 U/L). The frequency of cramping was greater in patients with elevated vs. normal CK (p < 0.0001).Discussion: HyperCKemia can occur in patients with peripheral neuropathy and appears to associate with cramping.

Complication Rates in Ankle and Hindfoot Charcot Arthropathy Treated with Arthrodesis

Category:Diabetes; Ankle; Hindfoot; OtherIntroduction/Purpose:Charcot arthropathy of the ankle and hindfoot is a progressive and destructive process that can lead to instability and ulceration resulting in significant morbidity. When indicated, the surgical goals are to restore a stable plantigrade foot, reduce the risk of ulceration, and improve function to independent ambulation. Techniques for reconstruction of the neuropathic ankle/hindfoot include external and/or internal fixation. Current literature involving small series of surgical patients has shown a high rate of limb salvage and low complication rate. Our experience has been less promising, although we believe it remains a viable option. It is our goal to report the outcomes of Charcot patients undergoing corrective ankle and hindfoot reconstruction.Methods:We retrospectively reviewed 377 patients undergoing hindfoot and ankle arthrodesis at our institution from 2006- 2017. 77 patients were identified that underwent arthrodesis for Charcot arthropathy, 51 of which met inclusion and exclusion criteria with a minimum one year follow up. 42 had internal fixation as their primary procedure (plate or nail) and 9 patients underwent external fixation with a multi-planar external fixator. Median follow up time was 4 years (IQR 2.97 years).Preoperatively, basic demographic variables, etiology of neuropathy, ulcer status, radiographic measurements, Brodsky classification, and presence of a viable talus were collected and analyzed. Postoperatively, we collected complications including infection, hardware failure, ulceration, recurrent deformity, and nonunion. Reoperation numbers and indications for reoperation were also collected. The primary outcome measure was limb salvage at final follow up. Secondary outcome measures were ambulatory and footwear/bracing status.Results:11 patients (20%) underwent amputation at final follow up and 26 (47.3%) achieved radiographic union, both of which did not vary by fixation type (p=0.67 and p=0.88). The primary reasons for amputation were persistent infection and non-union. 74.5% of patients developed a post-operative complication and 58.2% had at least one reoperation. 25.5% of patients developed a post- operative infection. Patients with a pre-operative ulceration were more likely to undergo external fixation (p=0.02), but amputation rates did not differ between groups (p>0.99). There was a trend toward increased risk of post-operative infection in the ulceration group (p=0.07). A pre-operative Meary’s angle >25° was more likely to undergo amputation (p=0.04) and less likely to achieve radiographic union (p=0.05). 75.9% of patients were ambulatory at final follow up.Conclusion:Our rates of amputation (20%), post-operative infection (25%), complications (74.5%) and non-union (52%) are higher than previously described. Previous literature has described a near 100% limb salvage rate, but in our report on a large series of Charcot patients undergoing hindfoot/ankle arthrodesis we describe an 80% limb salvage rate. Pre-operative Meary’s angle >25° was predictive of treatment failure.

Gigaxonin glycosylation regulates intermediate filament turnover and may impact giant axonal neuropathy etiology or treatment

Gigaxonin (also known as KLHL16) is an E3 ligase adaptor protein that promotes the ubiquitination and degradation of intermediate filament (IF) proteins. Mutations in human gigaxonin cause the fatal neurodegenerative disease giant axonal neuropathy (GAN), in which IF proteins accumulate and aggregate in axons throughout the nervous system, impairing neuronal function and viability. Despite this pathophysiological significance, the upstream regulation and downstream effects of normal and aberrant gigaxonin function remain incompletely understood. Here, we report that gigaxonin is modified by <italic>O</italic>-linked β-<italic>N</italic>-acetylglucosamine (O-GlcNAc), a prevalent form of intracellular glycosylation, in a nutrient- and growth factor–dependent manner. MS analyses of human gigaxonin revealed 9 candidate sites of O-GlcNAcylation, 2 of which — serine 272 and threonine 277 — are required for its ability to mediate IF turnover in gigaxonin-deficient human cell models that we created. Taken together, the results suggest that nutrient-responsive gigaxonin O-GlcNAcylation forms a regulatory link between metabolism and IF proteostasis. Our work may have significant implications for understanding the nongenetic modifiers of GAN phenotypes and for the optimization of gene therapy for this disease.

A Clinician's Approach to Peripheral Neuropathy.

Peripheral neuropathies are a group of disorders that affect the peripheral nervous system, for which hundreds of etiologies have been identified. This article presents a stepwise approach to the evaluation and workup of peripheral neuropathy, which starts with a detailed history of symptoms, family and occupational history, and a neurological as well as general physical exam. Pattern recognition of various neuropathies can help to build a differential diagnosis based on the presentation. Such patterns include acute versus chronic, primary demyelinating versus axonal, hereditary versus acquired, asymmetric versus symmetric, presence of facial palsies, sensory or motor predominant, and presence of prominent autonomic symptoms. Early categorization of the type of neuropathy can help focus the workup for peripheral neuropathy. Nerve conduction studies and electromyography (NCS/EMG) is the primary diagnostic tool in the evaluation of patients with large-fiber polyneuropathy. One of the most important roles of NCS/EMG is to help categorize polyneuropathy as primary axonal versus primary demyelinating. The finding of a primary demyelinating polyneuropathy narrows the differential diagnosis of polyneuropathy dramatically and increases the chances of finding a treatable etiology. Laboratory workup includes serum studies and potentially cerebrospinal fluid, genetic studies, immunological markers, and fat pad biopsy for select patients. Skin biopsy may be used to assess intraepidermal nerve fiber density if small-fiber neuropathy is suspected, and nerve biopsy may be useful in select cases. In recent years, magnetic resonance imaging and neuromuscular ultrasound have also shown promise in the evaluation of peripheral neuropathy. Identification of the etiology of neuropathy is crucial and often time-sensitive, as an increasing number of causes are now reversible or treatable.

MON-142 Neuropathy in a Patient with Diabetes Mellitus: Not Always a Diabetic Disease

Diabetic neuropathy (DN) is the most common form of neuropathy in patients with diabetes mellitus (DM). Although DN is very common, other etiologies for neuropathy can exist or co-exist in patients with DM. DN might be nonspecific and mimic neuropathies seen in other diseases. Therefore, its proper diagnosis requires a thorough history and exclusion of secondary causes such as leprosy. Due to increase in world-wide travel and migration, and because the transmission pathways of Mycobacterium leprae are not fully understood, it is now crucial to be aware of tropical diseases, such as leprosy, not generally seen or recognized in non-endemic countries. We report a case of 74-year old man with a 5-year history of DM who complained of feet paresthesia over the last four years, more pronounced on the left foot and progressively worse. Good glycemic control was achieved since diagnosis with Metformin. Microvascular complications were absent. Renal and thyroid function were normal as well as vitamin B12 levels. The patient denied alcohol or drug abuse, and did not have peripheral arterial disease, cancer, or use any neurotoxic drug. On examination of the lower limbs, deep tendon reflexes diminished. A mildly decreased vibration perception and numbness on the lower left limb were also observed. No other finding was present (normal pin-prick, normal gait and proprioception), nor did he present with muscle weakness. Amitriptyline and thioctic acid were prescribed with no clinical response. During the last year, multiple hyperpigmented anesthetic cutaneous lesions emerged in his legs and back. He subsequently developed a left foot drop and autonomic dysfunction. A diagnosis of borderline tuberculoid leprosy and type 1 reaction were established and a planned 12-month multidrug therapy (MDT) initiated. After six months of MDT, at last follow-up, the patient’s sensory neuropathy showed mild improvement. Resolution of autonomic symptoms was seen and nearly complete clearing of the skin lesions. In conclusion, leprosy and DM can cause progressive and irreversible nerve damage with similar clinical patterns. But, in cases of asymmetric neuropathy in a patient with DM, leprosy must be ruled out first before ascribing DM as the cause of the neuropathy. A thorough epidemiological history is mandatory to avoid misdiagnosis. If leprosy is not recognized and consequently left untreated, patients are at risk for permanent nerve damage. Leprosy is a potentially curable disease, contrary to DM. Other etiologies for neuropathy can exist in patients with DM.

Sweating disorders in mice with and without nerve lesions.

Hypersensitivity and altered sweating are often present in neuropathy patients. Nerve lesions are known to produce sudomotor dysfunctions but also patients suffering from complex regional pain syndrome, CRPS1-a condition without a nerve lesion-present with sweating disorders. Using proton nuclear magnetic resonance of sweat water, we quantified sweat output of mice suffering from a nerve lesion or a bone fracture without nerve lesion and correlated their sweating with behavioural paw hypersensitivity accessed in von Frey testings, water applications and weight-bearing measured with an incapacitance metre. Lesioned animals sweat less and are hypersensitive compared to healthy controls, as expected. Fractured animals on the injured side sweat less acutely after the injury but more in the chronic phase. They are hypersensitive acutely as well as chronically after the fracture. These findings resemble human bone trauma patients in the acute phase and CRPS patients in the chronic phase. Sweating disorders are present both in neuropathic animals and in those with a bone fracture without nerve lesions, and autonomic dysfunctions might be considered as an important component in the aetiology of neuropathies. Sweat output changes in mice after bone trauma, potentially indicative of posttraumatic processes leading to CRPS in humans.

Dejerine: The concept of peripheral neuropathy

Dejerine: The concept of peripheral neuropathy

An integrated perspective on diabetic, alcoholic, and drug-induced neuropathy, etiology, and treatment in the US.

Neuropathic pain (NeuP) is a syndrome that results from damaged nerves and/or aberrant regeneration. Common etiologies of neuropathy include chronic illnesses and medication use. Chronic disorders, such as diabetes and alcoholism, can cause neuronal injury and consequently NeuP. Certain medications with antineoplastic effects also carry an exquisitely high risk for neuropathy. These culprits are a few of many that are fueling the NeuP epidemic, which currently affects 7%–10% of the population. It has been estimated that approximately 10% and 7% of US adults carry a diagnosis of diabetes and alcohol disorder, respectively. Despite its pervasiveness, many physicians are unfamiliar with adequate treatment of NeuP, partly due to the few reviews that are available that have integrated basic science and clinical practice. In light of the recent Centers for Disease Control and Prevention guidelines that advise against the routine use of μ-opioid receptor-selective opioids for chronic pain management, such a review is timely. Here, we provide a succinct overview of the etiology and treatment options of diabetic and alcohol- and drug-induced neuropathy, three different and prevalent neuropathies fusing the combined clinical and preclinical pharmacological expertise in NeuP of the authors. We discuss the anatomy of pain and pain transmission, with special attention to key ion channels, receptors, and neurotransmitters. An understanding of pain neurophysiology will lead to a better understanding of the rationale for the effectiveness of current treatment options, and may lead to better diagnostic tools to help distinguish types of neuropathy. We close with a discussion of ongoing research efforts to develop additional treatments for NeuP.

Clinical Manifestations of Isolated Elevated Homocysteine-Induced Peripheral Neuropathy in Adults.

To characterize the clinical features of isolated elevated plasma homocysteine (eHcy)-induced peripheral neuropathy (IHIN) in adults. Charts of subjects with the diagnosis of IHIN who visited neuromuscular clinic from January 01, 2012 to September 30, 2014 were reviewed. Subjects with identifiable etiologies for neuropathy, such as B12/folate deficiency; metabolic, toxic, endocrinologic, infectious/inflammatory renal or liver diseases; or traumatic nerve injury, were excluded. Their clinical presentations were recorded and analyzed. Thirty subjects (age: 63.2 ± 14.8 years, 13 males) were included. They all had an isolated increased homocysteine level (15.4 ± 5.3 μmol/L) but normal levels of B12, folate, and methylmalonic acid. Of 30, 14 (46.7%) had numb feet, 11 (36.7%) had numb hands, 7 (23.3%) had pain in lower extremities, and 10 (33.3%) had tingling in feet. Distal sensory deficits were present in 18/30 (60%) patients. Distal limb weakness was seen in 4 and decreased tendon reflexes in 12 patients. Sensory deficits are predominant components of IHIN. Characterizing clinical features of IHIN would help better understand eHcy-related neuropathy and improve its management.

Vitamin B12 and Holotranscobalamin Levels in Diabetic Peripheral Neuropathy Patients

ABSTRACT Diabetic neuropathy is the most common and debilitating microvascular complication leading to nontraumatic amputations. Identifying the role of vitamin B12 in the etiology of neuropathy is crucial because simple vitamin B12 replacement may reverse neurologic symptoms if confirmed. Large proportion of vegetarians and patients on metformin have been associated with lowering of vitamin B12 levels. We have undertaken study on 60 vegetarian subjects between the age of 30 and 60 years, 20 healthy controls, 20 type 2 diabetes mellitus patients who were on metformin with peripheral neuropathy (DMWN), and 20 diabetics without peripheral neuropathy (DMWON). Vitamin B12, homocysteine, and folate levels were measured, and holotranscobalamin (holoTC) is also included, to improve the diagnosis of tissue vitamin B12 status, as holoTC is the biologically active fraction and more sensitive index of vitamin B12 status than total vitamin B12 itself. Complete history and clinical evaluation for neuropathy and electroneuromyography were recorded. Results In the DMWN group, vitamin B12 levels were significantly higher than in the DMWON group and controls [1013 (564-1501) pmol/l, 387 (245-731) pmol/l, and 305 (234-472) pmol/l respectively]. Similarly, serum holoTC was also found to be significantly higher in the DMWN [203.8 (129-300) pmol/l] group compared with the DMWON [94.4 (42.2-230.6) pmol/l] group and controls [74 (40-170) pmol/l]. Whereas mean levels of homocysteine and folate did not show any significant difference between groups, significant increase in fasting blood sugar and HbA1c was seen in the DMWN group compared with DMWON group and controls. Duration of diabetes is also significantly more in DMWN group compared with DMWON group. Conclusion We found that vitamin B12 and holoTC levels were high in patients with DMWN and DMWON groups compared with controls. Our study demonstrated that peripheral neuropathy was not associated with vitamin B12 deficiency in diabetics. These findings merit further research on a larger population to investigate into the cause of diabetic neuropathy, the factors involved, and benefit of vitamin B12 supplementation in these patients. Key messages Vitamin B12 status has no association with diabetic peripheral neuropathy. How to cite this article Noorjahan M, Madhavi K, Priscilla C, Jabeen SA. Vitamin B12 and Holotranscobalamin Levels in Diabetic Peripheral Neuropathy Patients. Indian J Med Biochem 2016;20(1):16-20.

Causes of neuropathy in patients referred as "idiopathic neuropathy".

The etiology of neuropathy was idiopathic in 20%-30% of patients despite thorough investigation, based on results from the 1980s and 1990s. Since then, new etiologies have been recognized, and skin biopsy has been used to confirm small-fiber neuropathy. The authors reviewed the charts of 373 patients with idiopathic neuropathy who were referred to a neuropathy center between 2002 and 2012. Among the 284 eligible patients, 93 (32.7%) remained idiopathic. The most common cause was impaired glucose metabolism (72 patients, 25.3%), including diabetes in 26 and prediabetes in 46. Other etiologies were chronic inflammatory demyelinating polyneuropathy (CIDP) in 57 (20%) and monoclonal gammopathy in 20 (7%), as well as toxic, Sjögren disease, celiac disease, other immune-mediated diseases, vitamin B12 deficiency, amyloidosis, vitamin B1 and B6 deficiency, vasculitis, hypothyroidism, hereditary, Lyme disease, and anti-sulfatide antibody. The major causes of undiagnosed neuropathies were impaired glucose metabolism, CIDP, and monoclonal gammopathies. Despite thorough evaluation 32.7% remained idiopathic. Muscle Nerve 53: 856-861, 2016.

Primary glaucoma etiology: current theories and researches

The article presents a review of latest researches related to various aspects of primary glaucoma and optic neuropathy etiology. The effect of somatic factors on glaucoma progression is described. Arguments in favor of the interrelation of glaucoma and neurodegenerative processes are presented. The genetic basis for the development of glaucoma and a variety of its conjoined syndromes is considered. Immunological mechanisms that initiate the programmed cell death are analyzed. The processes that influence the increase of trabecular meshwork retention are also described as well as its role in the glaucoma pathogenesis.

Fascicular ratio: a new parameter to evaluate peripheral nerve pathology on magnetic resonance imaging: a feasibility study on a 3T MRI system.

The objective of the study was to define and quantitatively evaluate the fascicular ratio (FR) on magnetic resonance imaging (MRI) in patients with peripheral neuropathies compared with healthy controls.Forty control subjects (20 women, 20 men; age, 44.6 ± 13.4 years) and 40 patients with peripheral neuropathy (22 women, 18 men; age, 50.3 ± 10.2 years) were examined with a standard 3T MRI protocol. With customized software (with semiautomatic and automatic interface), the hypointense and hyperintense areas of the peripheral nerves corresponding to fascicular and nonfascicular tissue were examined on T1-weighted sequences. The ratio of fascicular pixels to total pixels was called FR. Correlation with FR calculated on high-resolution ultrasound was performed. The statistical analysis included the Mann–Whitney U test of controls versus patients, the receiver operating characteristic (ROC) analysis, and the subgroup analysis of patients according to etiologies of neuropathy. Intraobserver and interobserver agreement was calculated based on the evaluation made by 3 readers. Finally, a complete automatic evaluation was performed.On MRI, FRs were significantly increased in patients compared with controls (FR, 76.7 ± 15.1 vs 56 ± 12.3; P < 0.0001 for the semiautomatic interface; and FR 66.3 ± 17.5 vs 47.8 ± 18.4; P < 0.0001 for the automatic interface). The increase in FR was caused mainly by an increase in the hypointense part of the nerve. This observation was valid for all causes of neuropathies. ROC analysis found an area under the curve of 0.75 (95% confidence interval, 0.44–0.81) for FR to discriminate neuropathy from control. The correlation coefficient between MRI and ultrasound was significant (r = 0.49; 95% confidence interval for r, 0.21–0.70; P = 0.012).With the semiautomated evaluation, the mean intraobserver agreement was good (K = 0.86). The interobserver agreements were also good (reader 1 vs reader 2, k = 0.71; reader 2 vs reader 3, k = 0.78; reader 3 vs reader 1, k = 0.71). There were no statistically significant differences between the results obtained using the 2 methods.FR calculation on MRI is feasible, and it may be used in adjunct to standard MRI evaluation in peripheral nerve disorders.

Peripheral neuropathy incidence in inflammatory bowel disease

Our aim was to determine the incidence of peripheral neuropathy in a population-based inflammatory bowel disease (IBD) cohort from Olmsted County, Minnesota. We retrospectively ascertained neuropathy incidence in a population-based cohort of adult persons newly diagnosed with IBD between 1940 and 2004 in Olmsted County, Minnesota, using the medical records linkage system of the Rochester Epidemiology Project. The Kaplan-Meier method was used to estimate the cumulative incidence of neuropathy. A total of 772 Olmsted County residents aged 18 to 91 years were diagnosed with IBD. After 12,476 person-years, 9 patients developed neuropathy, providing an overall incidence rate of 72 (95% confidence interval [CI] 33-137) cases per 100,000 IBD person-years. The cumulative incidence rates after 10, 20, and 30 years were 0.7% (95% CI 0.0%-1.3%), 0.7% (95% CI 0.0%-1.5%), and 2.4% (95% CI 0.6%-4.6%), respectively. Neuropathy was diagnosed after 1 to 44 years from IBD onset. Only 2 patients had active bowel disease at the time of neuropathy onset. The clinical spectrum consisted of 1) monophasic immune radiculoplexus neuropathy (comorbid diabetes in 2 of 4 patients) and 2) chronic distal sensorimotor polyneuropathy (comorbid diabetes in 2 of 5 patients). Our population-based study suggests that neuropathy is uncommon in the patient population of IBD. Radiculoplexus neuropathy and sensorimotor polyneuropathy were both observed, commonly during periods of bowel disease inactivity. Clinicians should consider other etiologies of neuropathy in patients with IBD.

Subacute Inflammatory Demyelinating Polyneuropathy Combined with Optic Neuritis

It was sometimes difficult to differentiate between acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) and subacute inflammatory demyelinating polyneuropathy (SIDP). The CNS involvement of these polyneuropathies has rarely reported in the literature. We present the case of a 42-year-old man who developed rapidly developing inflammatory demyelinating polyneuropathy followed by right optic neuritis. This case showed progressive motor weakness and sensory dysfunction with time to nadir at 8 weeks, demyelination in nerve conduction study, no other etiology of neuropathy, no relapse during follow-up of 18 months, good response to steroid and complete recovery which favor SIDP more than A-CIDP. We experienced the case of SIDP associated with optic neuritis.

Transient femoral neuropathy after knee ligament reconstruction and nerve stimulator‐guided continuous femoral nerve block: a case series

Patients often develop a severe, but transient, quadriceps amyotrophy following anterior cruciate ligament (ACL) reconstruction [1]. We investigated whether or not this amyotrophy could be related to a femoral neuropathy induced by a pneumatic tourniquet [2] or by a continuous femoral nerve block [3]. After approval from our local research ethics committee, we performed a clinical neurological examination and an electrophysiological study before surgery to exclude pre-existing femoral neuropathy. We defined postoperative femoral neuropathy as an axon loss > 20%, associated with an absent H-reflex of the femoral nerve and signs of denervation of the vastus medialis muscle. The H-reflex (or Hoffmann reflex) is a reflex reaction of muscles after incremental electrical stimulation of sensory fibres. Signs of denervation were scored as present when fibrillation potentials of the muscle were observed at rest [4]. In each case, a femoral nerve catheter was inserted with a nerve stimulator using Winnie’s classic technique [5], followed by spinal or general anaesthesia. Follow-up neurological examinations and an electrophysiological study were scheduled at 4 weeks and 6 months after the ACL repair. Seventeen ASA patients, of ASA physical status 1–2 and with a mean age of 26 years, completed the study. After surgery, all patients developed subjective weakness of the quadriceps muscle without neuropathic pain or paraesthesia; in 11 patients (65%), a significant reduction of the compound muscle action potentials was observed. Four patients (24%) had clinical criteria or electrophysiological signs of femoral neuropathy at 4 weeks but not at 6 months (Figs 8 and 9). Acute neurological lesions from all causes occur in 8–14% of patients postoperatively [6, 7] and usually resolve to between 0.2% and 0.6% within 6–9 months postoperatively [6–10]. The explanation for the higher incidence we found at 4 weeks might be that we conducted a systematic investigation of neurological lesions even when patients were asymptomatic. Our femoral neuropathies could be the result of the thigh tourniquets, which can produce a compression paralysis and muscle ischaemia [11]. The tourniquet times and pressures were in the upper limits of the usual recommendations. We may also have caused direct nerve trauma during the femoral nerve blocks. We confirmed with electrophysiological study that ACL reconstruction was followed by quadriceps amyotrophy in 11 patients; this muscle amyotrophy may be worsened by a femoral neuropathy. Further studies are needed to assess the incidence and aetiology of neuropathy according to the type of surgery and analgesia, as well as to assess the influence of these factors on recovery of quadriceps muscle strength after ACL reconstruction.