Distal Symmetric Sensorimotor Polyneuropathy Research Articles

Ayurvedic Treatment Modalities of Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy is the damage of the nerves due to the uncontrolled diabetes. It can affect any of the neurons can affect any of the neurons. Diabetic distal symmetric sensory and sensorimotor polyneuropathy is the most prevalent type of diabetic neuropathy. The symptoms appear as sensory loss, first in the toes and progressively moving up the legs, fingers, and arms over time. Tingling sensation, Burning sensation, Deep aching pain are other related symptoms. A patient age 54 years with diabetes for past 15 years, hypertension, dyslipidemia, complains of burning sensation of both feet (right>left), numbness, pricking pain, unsteadiness while walking, brownish red discolouration of both lower limbs. The symptoms were gradual in onset. Nerve Conduction Study showed axonal type of motor and sensory affecting peroneal nerve neuropathy. He admitted in Vaidyaratnam Ayurveda College Hospital, done Vibrotherm Neuropathy Analyzer and revealed small and large fibre neuropathy with severe loss of sensations. The main intention of the study is to improve the quality of life of the patient by reducing the symptoms that is disturbing his day today routine. Patient given with anti diabetic Ayurvedic formulations internally. Externally Rookshana, Vatahara, Brimhana treatments were done. After the treatment, Michigan neuropathy screening instrument, diabetic Neuropathy symptom score, Toronto clinical scoring system score were reduced. Neuropathy Analyzer showed mild to moderate loss of sensation. By adopting Prameha hara chikitsa coupled with Vata vyadhihara chikitsa, complications of diabetes can be managed. It is important to focus on diet and regimen since diabetes is a lifestyle disorder and, in ayurveda it is considered as an Anushangi Vyadhi.

Diabetic Sensorimotor Polyneuropathy: An Overview on Epidemiology, Risk Factors, Classification, Diagnosis, and Treatment.

Diabetic distal symmetric sensorimotor polyneuropathy (DSPN) is a common complication of diabetes with devastating consequences. Hyperglycaemia is the major aetiological factor, while emerging data demonstrate that cardiometabolic risk factors also contribute to its development. Diagnosis of DSPN involves interview of medical and neurological history, foot inspection, and sensory and motor function examination with specific tests such as temperature and pinprick perception for small nerve fibers, and vibration and light touch assessments for large nerve fibers. Management includes optimised glycaemic control, treatment of cardiovascular risk factors, and symptomatic treatment aiming at improving life quality. This article provides an overview on epidemiology, risk factors, classification, diagnosis and current treatment of DSPN.

Bone remodeling and responsiveness to mechanical stimuli in individuals with type 1 diabetes mellitus.

Type 1 diabetes mellitus (T1DM) has been linked to increased osteocyte apoptosis, local accumulation of mineralized lacunar spaces, and microdamage suggesting an impairment of the mechanoregulation network in affected individuals. Diabetic neuropathy might exacerbate this dysfunction through direct effects on bone turnover, and indirect effects on balance, muscle strength, and gait. However, the in vivo effects of impaired bone mechanoregulation on bone remodeling in humans remain underexplored. This longitudinal cohort study assessed consenting participants with T1DM and varying degree of distal symmetric sensorimotor polyneuropathy (T1DM, n = 20, median age 46.5yr, eight female) and controls (CTRL; n = 9, median age 59.0yr, four female) at baseline and 4-yr follow-up. Nerve conduction in participants with T1DM was tested using DPNCheck and bone remodeling was quantified with longitudinal high-resolution peripheral quantitative-computed tomography (HR-pQCT, 82μm) at the standard distal sites. Local trabecular bone formation (Tb.F) and resorption (Tb.R) sites were captured by implementing 3D rigid image registration of HR-pQCT images, and the mechanical environment across the bone microarchitecture at these sites was simulated using micro-finite element analysis. We calculated odds ratios to determine the likelihood of bone formation (ORF) and resorption (ORR) with increasing/decreasing strain in percent as markers for mechanoregulation. At the distal radius, Tb.F was 47% lower and Tb.R was 59% lower in T1DM participants compared with CTRL (P < .05). Tb.F correlated positively with nerve conduction amplitude (R=0.69, P < .05) in participants with T1DM and negatively with glycated hemoglobin (HbA1c) (R= -0.45, P < .05). Additionally, ORF was 34% lower and ORR was 18% lower in T1DM compared with CTRL (P < .05). Our findings represent in vivo evidence suggesting that bone remodeling in individuals with T1DM is in a state of low responsiveness to mechanical stimuli, resulting in impaired bone formation and resorption rates; these correlate to the degree of neuropathy and level of diabetes control.

Diabetic Distal Symmetric Sensorimotor Polyneuropathy: A Proposal of New Electrodiagnostic Evaluation.

Diabetic Distal Symmetric Sensorimotor Polyneuropathy: A Proposal of New Electrodiagnostic Evaluation.

Electrophysiological Investigations in DiabetıC Patients

Introduction: The aim of the study is to search proximal nerve involvement by using proximal root stimulation and possible autonomic neuropathy in type 2 diabetic patients with and without distal symmetric sensorimotor polyneuropathy (DSPN). Patients and Methods: Forty patients with type 2 diabetes and ten volunteers who had no history of diabetes and neuropathy were included. Diabetic patients were equally distributed into two groups according to nerve conduction studies (NCSs): First group comprised of with electrophysiologically confirmed DSPN and second group with normal NCSs. Electrophysiological tests included motor and sensory nerve conduction, needle electromyography, F-response, H-reflex, R-R interval, and sympathetic skin responses (SSRs) studies as well as lumbar root stimulation and cauda equina motor conduction time (CEMCT) calculation. Results: The patients with DSPN had significantly longer F-response latencies and had no H-reflex while H-reflex was observed in 35% of the patients in second group. In the first group, SSRs could not be obtained from both upper and lower limbs in 45% of the patients; however, in the second group, they were absent only in 10% of patients in lower limbs. R-R interval variability was significantly lower in both diabetic groups than volunteers. When compared to the volunteers, cauda equine motor conduction time was significantly prolonged in all diabetic patients, but there was no significant difference between the patient groups. Conclusions: CEMCT prolongation, absence of H-reflex, and decreased R-R interval abnormalities indicating dysautonomia were the most important findings of our study. These results show that early electrophysiological examinations using these methods are important in diabetic patients without polyneuropathy.

Median to ulnar nerve comparison on diagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy - A neurophysiological study.

<p style="text-align: justify;"><strong>Background and purpose </strong>&ndash; To analyze the utility of median nerve (MN) to ulnar nerve (UN) comparative parameters on the diagnosis of carpal tunnel syndrome (CTS) in diabetic patients with distal symmetrical sensorimotor polyneuropathy (DSMPNP). <br><br><strong>Methods</strong> &ndash; Patients who were referred to our electroneuromyography laboratory within the last two years were included. We compared the diagnostic accuracy values of traditional MN conduction parameters, and the MN-to-UN comparative tests on electrodiagnosis of CTS between the patients with DSMPNP involving the nerves of upper and lower extremities (UEI-positive group), and the ones without the involvement of upper extremities (UEI-negative group). <br><br><strong>Results</strong> &ndash; There were 64 upper extremities in the UEI-positive group and 70 patients in the UEI-negative group. The most accurate traditional parameter was MN distal motor latency (DML) with a diagnostic accuracy of 70.2% whereas the most accurate comparative technique was the second lumbricalinterosseous DML difference (2L-INT DMLD) with an accuracy of 81.3%. (p=0.03). In addition, when compared diagnostic accuracy values of MN parameters with their corresponding comparative parameters in the UEI-positive group which carries the major diagnostic challenges for detecting co-morbid CTS, MN to UN minimum F wave latency (mFWL) difference, SNAP amplitude ratio on the ring finger (RF), and 2L-INT DMLD had higher accuracy values than MN mFWL, MN SNAP amplitude on RF, and MN DML on lumbrical muscle, respectively (p&lt;0.05 for all comparisons). <br><br><strong>Conclusion</strong> &ndash; MN to UN comparative studies have high accuracy values in electrodiagnosis of CTS in DSMPNP. In particular, 2L-INT DMLD could be helpful to overcome the diagnostic difficulty in the presence of UEI as an additional conduction technique.</p>.

Diabetes Mellitus and Bell's Palsy.

The aim of the present brief review was to discuss Bell's palsy (BP) in diabetes mellitus (DM). The risk of BP is increased in DM. DM subjects with BP are more prone to severe facial nerve degeneration. Further characteristics of BP in DM include: a) infrequent taste impairment; b) more frequent and more marked facial nerve subclinical electrophysiological impairment; c) more frequent BR impairment; d) potentially concurrent distal symmetrical sensorimotor polyneuropathy; e) more frequent alternating BP with recurrent episodes affecting different sides of the face.

Diagnostic Tools, Biomarkers, and Treatments in Diabetic polyneuropathy and Cardiovascular Autonomic Neuropathy.

The various manifestations of diabetic neuropathy, including distal symmetric sensorimotor polyneuropathy (DSPN) and cardiovascular autonomic neuropathy (CAN), are among the most prevalent chronic complications of diabetes. Major clinical complications of diabetic neuropathies, such as neuropathic pain, chronic foot ulcers, and orthostatic hypotension, are associated with considerable morbidity, increased mortality, and diminished quality of life. Despite the substantial individual and socioeconomic burden, the strategies to diagnose and treat diabetic neuropathies remain insufficient. This review provides an overview of the current clinical aspects and recent advances in exploring local and systemic biomarkers of both DSPN and CAN assessed in human studies (such as biomarkers of inflammation and oxidative stress) for better understanding of the underlying pathophysiology and for improving early detection. Current therapeutic options for DSPN are (I) causal treatment, including lifestyle modification, optimal glycemic control, and multifactorial risk intervention, (II) pharmacotherapy derived from pathogenetic concepts, and (III) analgesic treatment against neuropathic pain. Recent advances in each category are discussed, including non-pharmacological approaches, such as electrical stimulation. Finally, the current therapeutic options for cardiovascular autonomic complications are provided. These insights should contribute to a broader understanding of the various manifestations of diabetic neuropathies from both the research and clinical perspectives.

The Effects of Type 1 Diabetes and Diabetic Peripheral Neuropathy on the Musculoskeletal System: A Case-Control Study.

Fracture risk is increased in type 1 diabetes (T1D). Diabetic neuropathy might contribute to this increased risk directly through effects on bone turnover and indirectly through effects on balance, muscle strength, and gait. We compared patients with T1D with (T1DN+, n=20) and without (T1DN-, n=20) distal symmetric sensorimotor polyneuropathy and controls (n=20). We assessed areal bone mineral density (aBMD) and appendicular muscle mass by dual-energy X-ray absorptiometry, microarchitecture by high-resolution peripheral quantitative tomography at the standard ultra-distal site and at an exploratory 14% bone length site at the tibia and radius, bone turnover markers, and muscle strength, gait, and balance by Short Physical Performance Battery (SPPB). At the standard ultra-distal site, tibial cortical porosity was 56% higher in T1DN+ compared with T1DN- (p=.009) and correlated positively with the severity of neuropathy (Toronto Clinical Neuropathy Score; r=0.347, p=.028) and negatively with nerve conduction amplitude and velocity (r=-0.386, p=.015 and r=-0.358, p=.025, respectively). Similar negative correlations were also observed at the radius (r=-0.484, p=.006 and r=-0.446, p=.012, respectively). At the exploratory 14% offset site (less distal), we found higher trabecular volumetric BMD (tibia 25%, p=.024; radius 46%, p=.017), trabecular bone volume (tibia 25%, p=.023; radius 46%, p=.017), and trabecular number (tibia 22%, p=.014; radius 30%, p=.010) in T1DN- compared with controls. Both CTX and PINP were lower in participants with TD1 compared with controls. No difference was found in aBMD and appendicular muscle mass. T1DN+ had worse performance in the SPPB compared with T1DN- and control. In summary, neuropathy was associated with cortical porosity and worse performance in physical tests. Our findings suggest that bone structure does not fully explain the rate of fractures in T1D. We conclude that the increase in the risk of fractures in T1D is multifactorial with both skeletal and non-skeletal contributions. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

Diabetic polyneuropathy: diagnosis, prevention, and treatment

The most common form of peripheral nervous system damage in diabetes mellitus is distal symmetric sensorimotor polyneuropathy (DSSMPN). Chronic hyperglycemia, dyslipidemia, and impaired microcirculation are considered to be the key mechanisms for the development of DSSMPN, but its pathogenesis is still unclear and continues to be studied. The paper analyzes the issues of diagnosis of DSSMPN and the effective principles of patient treatment. It also discusses the use of alpha-lipoic acid (ALA) as a drug for the pathogenetic treatment of DSSMPN and describes the results of clinical trials of its treatment with ALA preparations.

Diabetic polyneuropathy

Approximately one of three people with diabetes is affected by distal symmetric sensorimotor polyneuropathy (DSPN) which is associated with marked impairment in quality of life due to partly excruciating neuropathic pain on the one hand and painless foot ulcers on the other hand. The prevalence of painful DSPN may reach up to one quarter of patients with diabetes, while DSPN may be asymptomatic in up to half of the patients affected. Regrettably, DSPN still remains underdiagnosed. Typical neuropathic symptoms include pain, paresthesias and numbness particularly in the feet and calves. The management of DSPN includes three cornerstones: (1)lifestyle modification, causal treatment aimed at near-normoglycemia and multifactorial cardiovascular risk intervention, (2)pathogenesis-derived treatment and (3)symptomatic treatment of neuropathic pain. Multimodal pain treatment should not only aim at pain relief, but also allow for improvement in quality of sleep, mobility, and general quality of life.

Cardiovascular Autonomic Neuropathy and Distal Symmetric Sensorimotor Polyneuropathy: These Two Diabetic Microvascular Complications do not Invariably Co-Exist.

Cardiovascular autonomic neuropathy (CAN) and distal symmetrical sensorimotor polyneuropathy (DSPN) are serious microvascular complications of diabetes mellitus (DM). Their simultaneous development remains disputable. The aim of the present study was to examine the correlation between CAN and the presence/severity of DSPN in DM. Subjects with type 1 (group A: n=51; mean age 40.4 years) and type 2 DM (group B: n=153; mean age 64.6 years) were studied. Evaluation of DSPN was based on neuropathy disability score. Assessment of CAN was based on the battery of 4 standardized cardiovascular autonomic function tests. In group A, patients with moderate/severe DSPN exhibited a 12-fold higher likelihood of CAN in univariate analysis (p=0.035). However, significance was lost after adjustment for gender, age, DM duration, and haemoglobin A1c. In group A, likelihood for CAN did not correlate with the presence of mild DSPN in univariate and multivariate analysis. In group B, likelihood of CAN was similar in patients with mild and in those with moderate/severe DSPN compared with patients without DSPN in univariate and multivariate analysis. In between group comparison CAN was similarly distributed in the 2 groups (p for interaction=0.367), in patients with no, mild and moderate/severe DSPN. CAN does not always co-exist with degrees of DSPN, ranging from mild to moderate/ severe and is similarly distributed in T1DM and T2DM patients with mild and moderate/severe DSPN and in patients without DSPN.

Untangling a case of painful neuropathy

A 51-year-old right-handed man developed a sensory neuropathy with the sensation of walking on pebbles, and tight cramping pains in the calves requiring amitriptyline. Two months later, he became unsteady...

Comparative Analysis of Efficacy and Safety of Gabapentin Vs Amitriptyline in Patients of Peripheral Neuropathic Pain in Case of Diabetes Mellitus

Introduction: Diabetes mellitus frequently leads to development of peripheral neuropathies in almost 30-50% of patients and the most common type of neuropathy associated with this condition is Distal Symmetric Sensorimotor Polyneuropathy (DSPN). Gabapentin and Amitriptyline are two drugs frequently used for the treatment of neuropathic pain associated with type 2 diabetes. Aim of the study: The aim of this study was to compare efficacy and safety of Gabapentin and Amitriptyline in subjects of Type 2 diabetes mellitus with peripheral neuropathic pain. Material and Methods: A prospective, open, randomized, parallel group, comparative study was conducted in 60 patients coming to Department of Medicine, Rajindra Hospital attached to Government Medical College Patiala, to evaluate the efficacy and safety of Gabapentin and Amitriptyline in patients with diabetic peripheral neuropathic pain. The patients fulfilling the inclusion criteria were included in the study after taking written informed consent. The patients were divided into two groups of 30 cases each by simple randomization. Group I patients received Gabapentin 300 mg HS by oral route. Group II patients received Amitriptyline 25 mg HS by oral route. Therapeutic efficacy of both drugs, by using Michigan Neuropathy Screening Instrument (MNSI) was compared at the baseline and at the end of 4 months. Any adverse drug reactions of the respective drug observed in patient were also noted. All the observations thus made were statistically analysed using appropriate tests. Results: Baseline characteristics of the patients in two groups such as age, sex, duration of diabetes were similar (p>0.05). The mean age in group I and group II were 53.40±8.41 years and 57.17±8.55 years, respectively. There was statistically significant reduction in mean MNSI scores in questionnaire part and physical examination part in both the groups. Also, there was statistically significant difference between the two drugs in reducing mean MNSI score. Mean difference between two drugs in reducing MNSI score in history part (0.77±0.16, p<0.01) and physical examination part (0.75±0.19, p<0.01) favoured Gabapentin. No. of adverse drug reactions reported were significantly higher in Amitriptyline group, p value (<0.05) for the difference in ADRs between two drugs was statistically significant. Conclusion: In this study, we concluded that both drugs lead to improvement in signs and symptoms of diabetic neuropathy. Gabapentin was proved to be more efficacious than Amitriptyline. Gabapentin treated patient’s mean MNSI score at the study end point was significantly lower as compared to the Amitriptyline treated patient’s end-point score. Adverse drug reactions reported in our study were mild in both the groups and a significantly higher number of adverse effects were reported in the amitriptyline group. Dizziness and somnolence were two most commonly reported adverse drug reactions.

Uremic neuropathy: an overview of the current literature

Peripheral neuropathy is a disorder that affects the cell body, axon or myelin of motor or peripheral sensory neurons and occurs in 60-100% of patients who are submitted to dialysis due to chronic kidney disease. Uremic neuropathy (UN) is attributed to the accumulation of organic waste, evident in patients with reduced glomerular filtration rate. This review aims to make clinical characteristics of uremic neuropathy evident enabling early diagnosis and treatment. This is a literature review of articles published on PubMed over the last 10 years using "Uremic Neuropathy" as "Title/Abstract". A total of nine articles that met the inclusion criteria were included. UN is a distal symmetric sensorimotor polyneuropathy that occurs due to the accumulation of uremic toxins associated with an oxidative stress-related free radical activity. Hyperkalemia is thought to play an important role in its pathophysiology. Diagnosis depends on nerve conduction studies, and treatment includes dialysis or renal transplant. Clinical presentations of UN are broad and non-specific; nonetheless, it is important to detect early changes in order to avoid its progression. The earlier UN is diagnosed and treated, the more successful are the clinical outcomes.

Uremic neuropathy: an overview of the current literature.

Peripheral neuropathy is a disorder that affects the cell body, axon or myelin of motor or peripheral sensory neurons and occurs in 60-100% of patients who are submitted to dialysis due to chronic kidney disease. Uremic neuropathy is attributed to the accumulation of organic waste, evident in patients with reduced glomerular filtration rate. This review aims to make clinical characteristics of uremic neuropathy evident enabling early diagnosis and treatment. This is a literature review of articles published on PubMed over the last 10 years using "Uremic Neuropathy" as "Title/Abstract". A total of nine articles that met the inclusion criteria were included. UN is a distal symmetric sensorimotor polyneuropathy that occurs due to the accumulation of uremic toxins associated with an oxidative stress-related free radical activity. Hyperkalemia is thought to play an important role in its pathophysiology. Diagnosis depends on nerve conduction studies, and treatment includes dialysis or renal transplant. Clinical presentations of UN are broad and non-specific; nonetheless, it is important to detect early changes in order to avoid its progression. The earlier UN is diagnosed and treated, the more successful are the clinical outcomes.

Specifics of diagnosis and treatment of diabetic polyneuropathy in elderly patients

To study the specifics of diagnosis and treatment of diabetic polyneuropathy in elderly patients. Forty-two patients (22 men and 20 women, aged from 65 to 75 years) with diabetes mellitus type 2 and diabetic polyneuropathy were studied using the following psychometric scales: the Michigan Neuropathy Screening Instrument (MNSI), Neurological symptoms scale (NSS), Neuropathy Disability Score (NDS), the Numerical Rating Scale (NRS), Kaplan-Feinstein index (KFI), the Covi Anxiety Scale (COVI), the Recovery Locus of Control Scale (RLOC). Patients were divided into group 1 (n=24) treated with neuromultivit injections, along with standard treatment, and group 2 (n=18), which received standard treatment only. Patients were examined at baseline and one month after treatment. In elderly patients, diabetic distal symmetric sensorimotor polyneuropathy of moderate severity was comorbid mostly with cardio-vascular disease. Pain syndrome was associated with anxiety and significant direct correlation between anxiety and pain intensity was found. The level of motivation towards recovery was significantly lower and correlated with COVI scores. Injections of neuromultivit decrease the intensity of pain, improve the emotional state and increase the level of motivation towards recovery.

Clinical manifestations of nervous system impairments in diabetes mellitus

Diabetes mellitus is one of the frequent diseases. The article describes diabetic neuropathy as the actual problem of modern neurology. It also provides the classification of central and peripheral nervous system impairments in diabetes mellitus and detailed description of such diseases as distal symmetric sensorimotor polyneuropathy, diabetic encephalopathy, acute neuropsychic disorders, cerebrovascular diseases and features of cognitive impairment in diabetes mellitus. Great attention is paid to the tactics of managing patients with above forms. The role of alpha-lipoic acid products in the treatment of diabetic impairments of the nervous system is thoroughly considered.

The efficacy of cocarnit in diabetic neuropathy

To study the efficacy of the complex therapy, including cocarnit (group B vitamins, triphosadenine and nicotinamide), of diabetic neuropathy. Forty-one patients with diabetes mellitus type 2 and distal symmetric sensorimotor polyneuropathy were examined. Patients were divided into 2 groups. Patients of the main group (n=26) received complex therapy, including cocarnit, and patients of the comparison group (n=15) received standard treatment. The positive dynamics based on the VAS (р=0.0001), TSS (р=0.0001), NSS (р=0.001), NDS (р=0.0431), SF-36 (р=0.0008), electroneuromyographic results and glycated hemoglobin levels was observed in the main group. In patients of the comparison group, the positive dynamics was instable; the scores of clinical scales did not reach statistical significance. The results suggest the use of cocarnit in the complex treatment of patients with diabetic neuropathy.

Impaired peripheral nerve regeneration in type-2 diabetic mouse model.

Peripheral neuropathy is one of the most common and serious complications of type-2 diabetes. Diabetic neuropathy is characterized by a distal symmetrical sensorimotor polyneuropathy, and its incidence increases in patients 40years of age or older. In spite of extensive research over decades, there are few effective treatments for diabetic neuropathy besides glucose control and improved lifestyle. The earliest changes in diabetic neuropathy occur in sensory nerve fibers, with initial degeneration and regeneration resulting in pain. To seek its effective treatment, here we prepared a type-2 diabetic mouse model by giving mice 2 injections of streptozotocin and nicotinamide and examining the ability for nerve regeneration by using a sciatic nerve transection-regeneration model previously established by us. Seventeen weeks after the last injection, the mice exhibited symptoms of type-2 diabetes, that is, impaired glucose tolerance, decreased insulin level, mechanical hyperalgesia, and impaired sensory nerve fibers in the plantar skin. These mice showed delayed functional recovery and nerve regeneration by 2weeks compared with young healthy mice and by 1week compared with age-matched non-diabetic mice after axotomy. Furthermore, type-2 diabetic mice displayed increased expression of PTEN in their DRG neurons. Administration of a PTEN inhibitor at the cutting site of the nerve for 4weeks promoted the axonal transport and functional recovery remarkably. This study demonstrates that peripheral nerve regeneration was impaired in type-2 diabetic model and that its combination with sciatic nerve transection is suitable for the study of the pathogenesis and treatment of early diabetic neuropathy.