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Journal articles on the topic 'Diabetic neuropathies'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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1

Bogdanov, E. I., V. V. Talantov, and R. Z. Mukhamedzyanov. "Diabetic neuropathies." Neurology Bulletin XXXII, no. 3-4 (July 15, 2000): 59–67. http://dx.doi.org/10.17816/nb79487.

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Diabetic neuropathies (DN) are among the most frequent and serious complications of diabetes [57, 9]. The detection rate of DN in diabetic patients varies greatly depending on their type, selected clinical and instrumental diagnostic criteria and, according to various researchers, ranges from 10 to 90% [16, 33]. At the same time, 1/3 of the polyneuropathies recognized in the neurological clinic are diabetic. In about 10% of cases, neuropathic symptoms are key in the diagnosis of diabetes [25]. DN has not only severe subjective manifestations and pronounced impairments that are objectively detected in them, but also leads to the development of diabetic foot syndrome - the cause of 50 - 70% of cases of all non-traumatic amputations of the legs [3]. In addition, in patients with diabetic visceral autonomic neuropathy, the syndrome of "sudden death" is much more common, and the frequency of painless myocardial infarctions and ischemic strokes is high. Clinical variants of DN are often the main causes of reduced quality of life, disability and disability in patients with diabetes mellitus. It is extremely important to diagnose the early stage of DN, when it is easier to achieve a therapeutic effect through the earliest and most stable provision of optimal control of an adequate level of glycemia and the appointment of means of pathogenetic therapy. Isolation of forms of DN, their diagnosis, treatment and prevention is an urgent clinical task.

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2

Elafros, Melissa A., and Brian C. Callaghan. "Diabetic Neuropathies." CONTINUUM: Lifelong Learning in Neurology 29, no. 5 (October 2023): 1401–17. http://dx.doi.org/10.1212/con.0000000000001291.

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ABSTRACT OBJECTIVE This article provides an up-to-date review of the diagnosis and management of the most common neuropathies that occur in patients with diabetes. LATEST DEVELOPMENTS The prevalence of diabetes continues to grow worldwide and, as a result, the burden of diabetic neuropathies is also increasing. Most diabetic neuropathies are caused by hyperglycemic effects on small and large fiber nerves, and glycemic control in individuals with type 1 diabetes reduces neuropathy prevalence. However, among people with type 2 diabetes, additional factors, particularly metabolic syndrome components, play a role and should be addressed. Although length-dependent distal symmetric polyneuropathy is the most common form of neuropathy, autonomic syndromes, particularly cardiovascular autonomic neuropathy, are associated with increased mortality, whereas lumbosacral radiculoplexus neuropathy and treatment-induced neuropathy cause substantial morbidity. Recent evidence-based guidelines have updated the recommended treatment options to manage pain associated with distal symmetric polyneuropathy of diabetes. ESSENTIAL POINTS Identifying and appropriately diagnosing the neuropathies of diabetes is key to preventing progression. Until better disease-modifying therapies are identified, management remains focused on diabetes and metabolic risk factor control and pain management.

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Alalwee, Azza, Jonathan D. LeSar, Mina Ghassemi, Eugene Cheng, Steven Stuto, Lawrence Osher, Scott Bastian, Vincent J. Hetherington, and Jill Kawalec. "Foot Temperature Trends in Normal, Diabetic, and Neuropathic Foot Populations." Journal of the American Podiatric Medical Association 106, sp1 (January 1, 2016): 5. http://dx.doi.org/10.7547/8750-7315-2016.1.alalwee.

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INTRODUCTION AND OBJECTIVES: Patients with underlying peripheral neuropathy are subject to changes in foot temperature. (1,2) Of the many forms of neuropathy that affect the lower extremity, the most notable are those types associated with diabetes. The aim of this study was to look for differences in temperatures between uncomplicated diabetic, diabetic neuropathic, and non-diabetic neuropathic feet. METHODS: The feet of 75 subjects were divided into 3 groups: 1) normal (n=50 feet), 2) diabetic (n=50 feet), and 3) neuropathic (n=49 feet). The neuropathic group was further subdivided into diabetic neuropathies (n=20 feet) and non-diabetic neuropathies (n=29 feet). To properly assign subjects to groups, all participants underwent vibratory threshold testing with a biothesiometer. In addition, all diabetic subjects had added glycosylated hemoglobin (hemoglobin A1C) studies performed. Temperature measurements were recorded at nine distinct foot locations (six plantar and three dorsal). Data was statistically analyzed using the Kruskal-Wallis test. RESULTS: For five of the plantar pedal sites tested, temperatures in the diabetic foot were significantly greater than those for the normal controls (p<0.05). At most sites, temperatures in the diabetic foot population tended to be higher than those in both diabetic and non-diabetic neuropathic feet, with the differences between the diabetic foot and non-diabetic neuropathic foot being statistically significant at one dorsal and five plantar sites. Patients in the non-diabetic neuropathic group were not stratified according to their specific neuropathic types. CONCLUSIONS: Diabetic feet, with and without neuropathy, tend to be warmer than the feet of patients with other non-diabetic neuropathies. The finding of no statistical difference between non-neuropathic diabetic and neuropathic diabetic feet is unexpected in that a number of these patients were projected to have an autonomic system component. These null findings suggest the need to further investigate neuropathy solely determined by sensory testing versus tests for autonomic system involvement.

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4

Fisher, Morris A., Vijaya K. Patil, and Charles L. Webber. "Recurrence Quantification Analysis of F-Waves and the Evaluation of Neuropathies." Neurology Research International 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/183608.

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Electrodiagnostic (EDX) patterns of neuropathic dysfunction have been based on axonal/demyelinating criteria requiring prior assumptions. This has not produced classifications of desired sensitivity or specificity. Furthermore, standard nerve conduction studies have limited reproducibility. New methodologies in EDX seem important. Recurrent Quantification Analysis (RQA) is a nonlinear method for examining patterns of recurrence. RQA might provide a unique method for the EDX evaluation of neuropathies. RQA was used to analyze F-wave recordings from the abductor hallucis muscle in 61 patients with neuropathies. Twenty-nine of these patients had diabetes as the sole cause of their neuropathies. In the other 32 patients, the etiologies of the neuropathies were diverse. Commonly used EDX variables were also recorded. RQA data could separate the 29 patients with diabetic neuropathies from the other 32 patients (P<0.009). Statistically significant differences in two EDX variables were also present: compound muscle action potential amplitudes (P<0.007) and F-wave persistence (P<0.001). RQA analysis of F-waves seemed able to distinguish diabetic neuropathies from the other neuropathies studied, and this separation was associated with specific physiological abnormalities. This study would therefore support the idea that RQA of F-waves can distinguish between types of neuropathic dysfunction based on EDX data alone without prior assumptions.

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5

Said, Gérard. "Focal and multifocal diabetic neuropathies." Arquivos de Neuro-Psiquiatria 65, no. 4b (December 2007): 1272–78. http://dx.doi.org/10.1590/s0004-282x2007000700037.

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Diabetic neuropathy is the most common neuropathy in industrialized countries, with a remarkable range of clinical manifestations. The vast majority of the patients with clinical diabetic neuropathy have a distal symmetrical form that progress following a fiber-length dependent pattern, with predominant sensory and autonomic manifestations. This pattern of neuropathy is associated with a progressive distal axonopathy. Patients are exposed to trophic changes in the feet, pains and autonomic disturbances. Less often, diabetic patients may develop focal and multifocal neuropathy that includes cranial nerve involvement, limb and truncal neuropathies. This neuropathic pattern tends to occur after 50 years of age, mostly in patients with longstanding diabetes mellitus. The LDDP does not show any trend to improvement and either relentlessly progresses or remain relatively stable over years. Conversely the focal diabetic neuropathies, which are often associated with inflammatory vasculopathy on nerve biopsies, remain self limited, sometimes after a relapsing course.

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6

Kazamel, Mohamed, and Peter J. Dyck. "Sensory manifestations of diabetic neuropathies: Anatomical and clinical correlations." Prosthetics and Orthotics International 39, no. 1 (January 22, 2015): 7–16. http://dx.doi.org/10.1177/0309364614536764.

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Background: Diabetes mellitus is among the most common causes of peripheral neuropathy worldwide. Sensory impairment in diabetics is a major risk factor of plantar ulcers and neurogenic arthropathy (Charcot joints) causing severe morbidity and high health-care costs. Objective: To discuss the different patterns of sensory alterations in diabetic neuropathies and their anatomical basis. Study design: Literature review. Methods: Review of the literature discussing different patterns of sensory impairment in diabetic neuropathies. Results: The different varieties of diabetic neuropathies include typical sensorimotor polyneuropathy (lower extremity predominant, length-dependent, symmetric, sensorimotor polyneuropathy presumably related to chronic hyperglycemic exposure, and related metabolic events), entrapment mononeuropathies, radiculoplexus neuropathies related to immune inflammatory ischemic events, cranial neuropathies, and treatment-related neuropathies (e.g. insulin neuritis). None of these patterns are unique for diabetes, and they can occur in nondiabetics. Sensory alterations are different among these prototypic varieties and are vital in diagnosis, following course, treatment options, and follow-up of treatment effects. Conclusions: Diabetic neuropathies can involve any segment of peripheral nerves from nerve roots to the nerve endings giving different patterns of abnormal sensation. It is the involvement of small fibers that causes positive sensory symptoms like pain early during the course of disease, bringing subjects to physician’s care. Clinical Relevance This article emphasizes on the fact that diabetic neuropathies are not a single entity. They are rather different varieties of conditions with more or less separate pathophysiological mechanisms and anatomical localization. Clinicians should keep this in mind when assessing patients with diabetes on the first visit or follow-up.

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7

Ward, J. D. "Diabetic Neuropathies." Drugs 32, no. 3 (September 1986): 279–89. http://dx.doi.org/10.2165/00003495-198632030-00004.

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8

Vinik, A. I., M. T. Holland, J. M. L. Beau, F. J. Liuzzi, K. B. Stansberry, and L. B. Colen. "Diabetic Neuropathies." Diabetes Care 15, no. 12 (December 1, 1992): 1926–75. http://dx.doi.org/10.2337/diacare.15.12.1926.

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9

Russell, James W., and Lindsay A. Zilliox. "Diabetic Neuropathies." CONTINUUM: Lifelong Learning in Neurology 20 (October 2014): 1226–40. http://dx.doi.org/10.1212/01.con.0000455884.29545.d2.

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10

Perkins, Bruce, Vera Bril, and Aaron Izenberg. "Diabetic Neuropathies." Seminars in Neurology 35, no. 04 (October 6, 2015): 424–30. http://dx.doi.org/10.1055/s-0035-1558972.

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11

Wein, Theodore H., and James W. Albers. "Diabetic Neuropathies." Physical Medicine and Rehabilitation Clinics of North America 12, no. 2 (May 2001): 307–20. http://dx.doi.org/10.1016/s1047-9651(18)30071-8.

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12

Vinik, A. I., and Anahit Mehrabyan. "Diabetic neuropathies." Medical Clinics of North America 88, no. 4 (July 2004): 947–99. http://dx.doi.org/10.1016/j.mcna.2004.04.009.

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13

Sinnreich, Michael, Bruce V. Taylor, and P. James B. Dyck. "Diabetic Neuropathies." Neurologist 11, no. 2 (March 2005): 63–79. http://dx.doi.org/10.1097/01.nrl.0000156314.24508.ed.

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14

Sima, A. A. F., P. K. Thomas, D. Ishii, and A. Vinik. "Diabetic neuropathies." Diabetologia 40 (September 19, 1997): S74—S77. http://dx.doi.org/10.1007/s001250051409.

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15

Vinik, A. I., T. S. Park, K. B. Stansberry, and G. L. Pittenger. "Diabetic neuropathies." Diabetologia 43, no. 8 (August 9, 2000): 957–73. http://dx.doi.org/10.1007/s001250051477.

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16

Zochodne, Douglas W. "Diabetic neuropathies." Current Treatment Options in Neurology 2, no. 1 (January 2000): 23–29. http://dx.doi.org/10.1007/s11940-000-0021-2.

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17

Skljarevski, Vladimir, and Alberto Lledo. "Diabetic Neuropathies." Archives of Neurology 63, no. 10 (October 1, 2006): 1502. http://dx.doi.org/10.1001/archneur.63.10.1502.

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18

Weber, Gerald A., and Mary Ann Cardile. "Diabetic Neuropathies." Clinics in Podiatric Medicine and Surgery 7, no. 1 (January 1990): 1–36. http://dx.doi.org/10.1016/s0891-8422(23)00360-9.

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19

Sima, A. A. F., P. K. Thomas, D. Ishii, and A. Vinik. "Diabetic neuropathies." Diabetologia 40, S3 (March 1997): B74—B77. http://dx.doi.org/10.1007/bf03168192.

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20

Patel, Kamakshi, Holli Horak, and Ezgi Tiryaki. "Diabetic neuropathies." Muscle & Nerve 63, no. 1 (July 28, 2020): 22–30. http://dx.doi.org/10.1002/mus.27014.

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21

Boulton, A. J. M., R. A. Malik, J. C. Arezzo, and J. M. Sosenko. "Diabetic Somatic Neuropathies." Diabetes Care 27, no. 6 (May 25, 2004): 1458–86. http://dx.doi.org/10.2337/diacare.27.6.1458.

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22

Baba, Masayuki. "3. Diabetic Neuropathies." Nihon Naika Gakkai Zasshi 98, no. 4 (2009): 779–86. http://dx.doi.org/10.2169/naika.98.779.

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23

Harati, Y. "Diabetic Peripheral Neuropathies." Methodist DeBakey Cardiovascular Journal 6, no. 2 (April 1, 2010): 15. http://dx.doi.org/10.14797/mdcvj.199.

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24

HARATI, YADOLLAH. "Diabetic Peripheral Neuropathies." Annals of Internal Medicine 107, no. 4 (October 1, 1987): 546. http://dx.doi.org/10.7326/0003-4819-107-4-546.

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25

Harati, Y. "Diabetic Peripheral Neuropathies." Methodist DeBakey Cardiovascular Journal 6, no. 2 (April 2010): 15–19. http://dx.doi.org/10.14797/mdcj-6-2-15.

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26

Gooch, Clifton, and David Podwall. "The Diabetic Neuropathies." Neurologist 10, no. 6 (November 2004): 311–22. http://dx.doi.org/10.1097/01.nrl.0000144733.61110.25.

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27

Alkatib, Ahed J. "DIABETES AND DIABETIC NEUROPATHIES ARE INDEPENDENT EVENTS: A NEW MEDICAL HYPOTHESIS." INDIAN RESEARCH JOURNAL OF PHARMACY AND SCIENCE 4, no. 3 (September 2017): 1064–67. http://dx.doi.org/10.21276/irjps.2017.4.3.2.

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28

M. H., Siddesh Kumar, Moosabba M. S., and Sanjay N. Koppad. "A study on peripheral neuropathy in patients with diabetic foot ulcers." International Surgery Journal 5, no. 3 (February 26, 2018): 913. http://dx.doi.org/10.18203/2349-2902.isj20180802.

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Background: Diabetic neuropathies are nerve disorders associated with diabetes. The most common complication of diabetes is caused by hyperglycemia which can damage nerve fibers throughout the body. Depending on the types of nerves involved, diabetic neuropathies can be categorized as peripheral, autonomic, proximal, focal neuropathies.Methods: A total of 62 diabetic foot patients admitted in general surgery department of Yenepoya medical college and hospital undergo neurological examination. Patients who were having peripheral neuropathy with diabetic foot ulcer between 18 and 85 years of age were included in the study.Results: On 62 patients with diabetic foot ulcers, 50 were unilateral and 12 were bilateral among which 8 patients had undergone toe amputation prior to examination. Patients were predominantly male 48 (77.4%). There were 14 women and 48 men with an average duration of diabetics being 15.6 and 14.8 years respectively. Women were older than male patient (58.2 v/s 51.7 years). Study of motor and sensory signs men and women patients, abnormal deep tendon reflex and deep sensory loss was high. Abnormal deep tendon reflex was 38 (79.1%) and 11 (78.5%), atrophy was 24 (50%) and 2 (14.2%), loss of pain was 18 (37%) and 4 (28.5%), loss of touch was 32 (66%) and 8 (57%), and deep sensory loss was 42 (87.5%) and 12 (85.7%) in men and women respectively.Conclusions: Diabetes mellitus leads to neuropathies of more than one type and all contribute to diabetic foot pathogenesis. Clinical symptoms and signs, as well as nerve conduction studies may be different between men and women with diabetic foot. Motor neuropathies may constitute an important prognostic parameter in men. Mononeuropathies sometimes reflect more severe involvement and peroneal and ulnar neuropathy is remarkable among these.

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29

Khramilin, V. N. "Differential diagnosis of polyneuropathies in diabetes mellitus." Meditsinskiy sovet = Medical Council, no. 12 (September 19, 2021): 256–65. http://dx.doi.org/10.21518/2079-701x-2021-12-256-265.

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Diabetic polyneuropathy (DPN) is heterogeneous in its clinical course and clinical manifestations. Depending on the primary lesion of large or small nerve fibers, different onset, course and clinical manifestations of polyneuropathy are possible. In patients with diabetes, the incidence of associated lesions of the peripheral nervous system is high. When verifying the diagnosis of DPN, it is necessary to carry out a differential diagnosis with a number of diseases: paraneoplastic neuropathies, metabolic neuropathies, neuropathies in vasculitis, toxic neuropathies, autoimmune neuropathies, inflammatory neuropathies and hereditary neuropathies. Diabetes is not the only cause of polyneuropathy. Up to 50% of all cases of polyneuropathies in diabetes have additional causes. Diagnosis of diabetic polyneuropathy - diagnosis of exclusion. The development of polyneuropathy in patients with a duration of type 1 diabetes less than 5 years, the absence of nephropathy and / or retinopathy, asymmetry in symptoms and signs, the predominance of motor symptoms, beginning with upper limb lesions, rapid progression should justify the doctor for differential diagnostic search. You should also take into account the characteristics of the patient (old age, vegetarianism and alcohol use), medical and toxic effects (taking metformin> 3 years and> 2 g / day; cytostatics, chemotherapy, heavy metals), family history of neuropathy. Therapeutic tactics should be individualized and take into account the polyneuropathy polyetiology. The purpose of this review is to discuss the most common reasons peripheral neuropathy in diabetes mellitus. The differential diagnosis of the diabetic polyneuropathy is the focus of this article.

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30

Zakin, Elina, Rory Abrams, and David M. Simpson. "Diabetic Neuropathy." Seminars in Neurology 39, no. 05 (October 2019): 560–69. http://dx.doi.org/10.1055/s-0039-1688978.

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AbstractDiabetes mellitus is becoming increasingly common worldwide. As this occurs, there will be an increase in the prevalence of known comorbidities from this disorder of glucose metabolism. One of the most disabling adverse comorbidities is diabetic neuropathy. The most common neuropathic manifestation is distal symmetric polyneuropathy, which can lead to sensory disturbances, including diminished protective sense, making patients prone to foot injuries. However, focal, multifocal, and autonomic neuropathies are also common. Diabetic nerve pain and Charcot osteoarthropathy are advanced neuropathic conditions that portend a severe deterioration in quality of life. To combat these symptoms, along with glycemic control and establishment of health care systems to educate and support patients with the complexities of diabetes, there are pharmacologic remedies to ameliorate the neurologic symptoms. Several guidelines and review boards generally recommend the use of tricyclic antidepressants, serotonin/norepinephrine-reuptake inhibitors, α-2-delta ligands, and anticonvulsants as medications to improve painful diabetic neuropathy and quality of life.

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31

Okada, S., S. Tanokuchi, K. Ishii, H. Hamada, K. Ichiki, Z. Ota, M. Shimizu, Y. Hirakt, and H. Nagashima. "Diversity of the Neuropathies in Patients with Non-Insulin-Dependent Diabetes Mellitus." Journal of International Medical Research 24, no. 1 (January 1996): 122–31. http://dx.doi.org/10.1177/030006059602400116.

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The relationships between cardiac autonomic neuropathies, diabetic somatic neuropathy, metabolic parameters, general parameters (such as age and duration of illness) and diabetic microangiopathy and macroangiopathy were investigated in 103 patients with non-insulin-dependent diabetes mellitus (NIDDM). Spearman's correlation coefficients were calculated for the comparisons of all the parameters of the neuropathies with all the other parameters. Variables were selected using a stepwise procedure and multiple regression analysis was carried out using these variables. The results of the regression analysis show that diabetic neuropathy is correlated with vascular parameters including blood pressure and pulse-wave velocity, as well as with parameters of sugar and lipid metabolism. The results confirm the diversity of the clinical characteristics of the neuropathies in patients with NIDDM and confirm that these neuropathies do not always occur in parallel.

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32

Dillon, Brendan R., Lynn Ang, and Rodica Pop-Busui. "Spectrum of Diabetic Neuropathy: New Insights in Diagnosis and Treatment." Annual Review of Medicine 75, no. 1 (January 29, 2024): 293–306. http://dx.doi.org/10.1146/annurev-med-043021-033114.

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Diabetic neuropathy is a highly prevalent complication of diabetes. It consists of a broad range of neuropathic conditions, such as distal symmetric polyneuropathy and various forms of autonomic neuropathies involving the cardiovascular, gastrointestinal, and urogenital systems. Prevention or diagnosis in early stages of disease is crucial to prevent symptomatic onset and progression, particularly in the absence of current disease-modifying therapies. In this review, we describe the four main types of diabetic neuropathy. We review current understanding with respect to diagnosis and treatment while highlighting knowledge gaps and future directions.

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33

Abrams, Paris J. "Pharmacologic Treatments for Pain Associated With Diabetic Peripheral Neuropathies." Journal of Pharmacy Practice 20, no. 1 (February 2007): 103–9. http://dx.doi.org/10.1177/0897190007304831.

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Diabetic peripheral neuropathy (DPN) is a complication of diabetes mellitus that occurs in both type 1 and type 2 diabetics. This complication is estimated to be prevalent in approximately 50% of the diabetic population and is associated with significant morbidity and mortality. Painful DPNs affect a minority of patients with DPN but are often chronic, severe, and debilitating. Many pharmacologic agents—including but not limited to pregabalin, duloxetine, tricyclic antidepressants, abapentin, and carbamazepine—have been studied and proven effective for the treatment of pain associated with DPN. Data from these studies were extracted and evaluated to compile a list of agents that are effective in treating painful diabetic neuropathies.

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34

Sharma, Kapil, Amit Varma, and Sumita Sharma. "Evaluation of diabetic neuropathies." Journal of Cardio-diabetes and metabolic disorders 2, no. 1 (2022): 9. http://dx.doi.org/10.4103/jcdm.jcdm_2_22.

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35

Tracy, Jennifer A., and P. James B. Dyck. "Managing inflammatory diabetic neuropathies." Diabetes Management 4, no. 5 (September 2014): 437–48. http://dx.doi.org/10.2217/dmt.14.32.

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36

Deguchi, Takahisa, and Yoshihiko Nishio. "IV. Diabetic Peripheral Neuropathies." Nihon Naika Gakkai Zasshi 108, no. 8 (August 10, 2019): 1538–44. http://dx.doi.org/10.2169/naika.108.1538.

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37

Boulton, A. J. M., and J. D. Ward. "Diabetic neuropathies and pain." Clinics in Endocrinology and Metabolism 15, no. 4 (November 1986): 917–31. http://dx.doi.org/10.1016/s0300-595x(86)80080-9.

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38

Sasaki, Hideyuki, Nobutoshi Kawamura, Peter J. Dyck, P. James B. Dyck, Mikihiro Kihara, and Phillip A. Low. "Spectrum of diabetic neuropathies." Diabetology International 11, no. 2 (January 8, 2020): 87–96. http://dx.doi.org/10.1007/s13340-019-00424-7.

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39

Harati, Yadollah. "Diabetic Neuropathies: Unanswered Questions." Neurologic Clinics 25, no. 1 (February 2007): 303–17. http://dx.doi.org/10.1016/j.ncl.2007.01.002.

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40

Brown, Mark J., and J. Richard Baringer. "Differentiating the Diabetic Neuropathies." Hospital Practice 29, no. 4 (April 15, 1994): 37–44. http://dx.doi.org/10.1080/21548331.1994.11443001.

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41

Said, Gérard. "Inflammation in Diabetic Neuropathies." European Neurological Review, no. 1 (2006): 73. http://dx.doi.org/10.17925/enr.2006.00.01.73.

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42

Golovacheva, V. A. "Early diagnosis and treatment of diabetic and alcoholic polyneuropathy in outpatient practice." Neurology, Neuropsychiatry, Psychosomatics 12, no. 6 (December 12, 2020): 96–103. http://dx.doi.org/10.14412/2074-2711-2020-6-96-103.

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Diabetes mellitus (DM) and chronic alcoholism (CA) are diseases that damage many organs and systems of the body and, in particular, lead to peripheral neuropathies. The pathogenesis of peripheral neuropathies caused by diabetes mellitus (DM) and CA is complex and diverse. Different types of peripheral neuropathies develop according to the leading pathogenetic mechanism. The most common type of peripheral neuropathy in DM is diabetic distal symmetric polyneuropathy (DSPN) and that in CA is alcoholic polyneuropathy (APN). The principles of diagnosis and treatment of DSPN and APN are considered. Treatment of DSPN and APN is complex, which is aimed at treating the underlying disease and includes non-drug and drug treatments. The mainstay of DSPN treatment is achievement of the optimal blood glucose level, maintenance of a healthy lifestyle (diet, daily activity), and correction of cardiovascular comorbidities (if any) with symptomatic pharmacotherapy for neuropathic pain (if any) with antidepressants or anticonvulsants. Antioxidants, such as B group vitamins (B1, B6 and B12) and alpha-lipoic acid (ALA), are widely used to treat DSPN in clinical practice. APN treatment involves cessation of alcohol consumption, physical and mental rehabilitation, and intake of B group vitamins (B1, B2, B6 and B12). The use of ALA in DSPN and APN is discussed.

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43

Serhiyenko, Victoria, Ludmila Serhiyenko, and Alexandr Serhiyenko. "Alpha-lipoic acid and diabetic cardiac autonomic neuropathy." MOJ Public Health 8, no. 1 (January 18, 2019): 8–10. http://dx.doi.org/10.15406/mojph.2019.08.00276.

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Alpha-lipoic acid (ALA) supplementation may provide benefits in the prevention of diabetes-related vascular and neuronal comorbidities. The mechanism of ALA influence on diabetic neuropathies pathogenesis is not well-known. Thus, further investigations aimed to understand the mechanism of action and for confirmation of the beneficial effect of ALA on biochemical parameters, dynamics of independent cardiovascular tests daily, monitoring of electrocardiography, arterial wall stiffness parameters among patients with type 2 diabetes mellitus, diabetic neuropathies and its associated comorbidities may be needed to validate this clinical findings.

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44

Di Stefano, Giulia, Andrea Di Lionardo, Giuseppe Di Pietro, and Andrea Truini. "Neuropathic Pain Related to Peripheral Neuropathies According to the IASP Grading System Criteria." Brain Sciences 11, no. 1 (December 22, 2020): 1. http://dx.doi.org/10.3390/brainsci11010001.

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Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system. Neuropathic pain represents a broad category of pain conditions, common complications of peripheral neuropathies, which are characterized by a combination of positive symptoms, including paresthesia and/or dysesthesia and sensory deficits in the painful area. In the present paper, we aimed to assess neuropathic pain frequency and clinical characteristics of peripheral neuropathies due to different aetiologies according to grading system criteria of the International Association for the Study of Pain for a definitive diagnosis of neuropathic pain. Epidemiological studies applying these criteria have been conducted in patients with diabetes, brachial plexus injury, and other traumatic nerve injuries. Neuropathic pain was diagnosed in 37–42% of patients with diabetic peripheral neuropathy, 56% of patients with brachial plexus injury, and 22% of patients with intercostobrachial neuropathy. The most frequent neuropathic pain type was ongoing pain (described as burning or pressing), followed by paroxysmal pain (electric shock-like sensations) and allodynia (pain evoked by brushing and pressure). By providing information on the frequency, clinical signs, and variables associated with neuropathic pain due to different aetiologies, these studies contribute to improving the clinical management of this condition.

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Akhmedzhanova, L. T., A. N. Barinov, and I. A. Strokov. "Diabetic and non-diabetic neuropathies in patients with diabetes mellitus." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 118, no. 4 (2018): 113. http://dx.doi.org/10.17116/jnevro201811841113-120.

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Pizova, N. V. "Main types of diabetic neuropathies." Consilium Medicum 20, no. 4 (2018): 36–42. http://dx.doi.org/10.26442/2075-1753_2018.4.36-42.

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Tomlinson, David R., and Natalie J. Gardiner. "Diabetic neuropathies: components of etiology." Journal of the Peripheral Nervous System 13, no. 2 (June 2008): 112–21. http://dx.doi.org/10.1111/j.1529-8027.2008.00167.x.

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Deli, Gabriella, Edit Bosnyak, Gabriella Pusch, Samuel Komoly, and Gergely Feher. "Diabetic Neuropathies: Diagnosis and Management." Neuroendocrinology 98, no. 4 (2013): 267–80. http://dx.doi.org/10.1159/000358728.

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Tracy, Jennifer A., and P. James B. Dyck. "The Spectrum of Diabetic Neuropathies." Physical Medicine and Rehabilitation Clinics of North America 19, no. 1 (February 2008): 1–26. http://dx.doi.org/10.1016/j.pmr.2007.10.010.

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Zochodne, Douglas W. "Diabetic Neuropathies: Features and Mechanisms." Brain Pathology 9, no. 2 (April 5, 2006): 369–91. http://dx.doi.org/10.1111/j.1750-3639.1999.tb00233.x.

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