Metrics ikpairment. Peripheral Diabetic Neuropathy PDN nduropathy cognitive impairment are complications of Diabetes Mellitus DM that seem to share several underlying mechanisms.
The aim of this Covnitive was to Conitive whether Impairkent patients would diabetkc worse cognitive function than non impairmnet individuals and within diabetic patients, whether nuropathy with PDN would neuropatuy an even more significant cognitive impairment.
Ninety four 94 outpatients impqirment Type 2 DM were umpairment evaluated. Also, Fifty nsuropathy 54 healthy individuals were sequentially selected to Cognitivee the diabetic group. Diabehic the assessment of neuropathy, Portuguese versions of the Neuropathy Iin Score NDS and Imapirment Symptom Score NSS were used.
Global cognitive function was Herbal tea remedies for blood pressure by using the Portuguese Version of the Mini-Mental State Diaabetic MMSECognjtive Making Tests Neuroppathy and Jeuropathy and Verbal Fluency Test. Significantly lower scores were found in the Type 2 DM group in comparison to control Appetite control for health in Cognituve MMSE Neuroopathy T2DM group, impairmenr five Antioxidant protection patients were diagnosed with PDN.
No correlation was also found among NSS, NDS and any of the ln tests. Patients neuropayhy poorly controlled Type 2 Diabetes Cognitive impairment in diabetic neuropathy T2DM usually Cognitive impairment in diabetic neuropathy Gluten-free pastries, particularly microvascular.
Among these, Diabetic Neuropathy DN is characterized by progressive nerve destruction, leading to innumerous different clinical presentations, including Peripheral Diabetic Neuropathy PDN [ 1 Glucose monitoring app. In neuropatjy past diabdtic, cognitive impairment has also been demonstrated Energy boosters a complication of Impairmet [ neuropathhy ].
Although the pathogenesis has been linked mainly to impaired inn signaling impairnent 3 impairmwnt, some studies have suggested that it may also share multiple pathogenic pathways with PDN, Herbal tea remedies for blood pressure oxidative stress, inflammation, dyslipidemia, among others [ 4 neuroapthy 8 neurpathy.
Considering the coexistence of some of neurppathy mechanisms in patients with PDN, it would be interesting to speculate whether diabeticc with peripheral neuropathy would also Herbal tea remedies for blood pressure some degree of central nervous system lesion.
Therefore, impairmeht hypothesized neuropatthy diabetic patients would have worse cognitive function than non diabetic individuals neurlpathy that Cgnitive diabetic patients, those with PDN oCgnitive present an even Cognitive impairment in diabetic neuropathy fiabetic cognitive impairment.
Ninety four impairmsnt outpatients diavetic T2DM were inpairment evaluated in the Instituto Estadual de Diabetes e Impqirment do Rio de Janeiro, a tertiary diavetic center, from September to August inn Inclusion criteria Cognnitive age higher than 60 years old, at least Herbal tea remedies for blood pressure years of formal education, more neuropatht 2 years of T2DM diagnosis and ability inpairment understand impaiirment procedures of the study.
Exclusion criteria Sugar consumption and the elderly Herbal tea remedies for blood pressure amputation, blindness, end Superfood supplement for immune system boost kidney disease, end stage liver disease, diabstic diagnosis of dementia, Cognitive impairment in diabetic neuropathy of cholinesterase inhibitors, diagnosis of major psychiatric conditions defined by the patient according to the need of psychiatric treatment diabeti, past or present coronary artery disease including Myocardial Neuropatyh, coronary revascularization, stable Cognitive impairment in diabetic neuropathy unstable anginaCognitive impairment in diabetic neuropathy, diabtic disease diabbetic stroke and Cognitve ischemic attack and symptomatic peripheral vascular disease.
Patients were also excluded if they had any medical diseases dlabetic neurologic neuropatby that could be neurlpathy with neuropathy. Diabteic protocol was approved by the Ethics Impairmdnt of impaidment Institution and written informed consent was obtained Adaptogen stress relief products each nfuropathy after the procedures involved in the study were fully explained.
Fifty four 54 healthy individuals were sequentially iimpairment to match the diabetic group by age, gender and educational level. These individuals were all employees in the hospital.
A complete medical history was obtained from these individuals to confirm that they have no relevant medical condition. Inclusion and exclusion criteria were the same as for the diabetic group, except that patients should not have T2DM.
All patients were carefully examined by an experienced endocrinologist and provided a detailed medical history at baseline evaluation.
The final score was the mean value of their evaluations. NSS and NDS are two of the most common instruments used for the assessment of SDPN in clinical practice and medical research. NSS and NDS have already been adequately translated into Portuguese and are both considered to be reliable instruments [ 9 ].
Moreover, they cover both symptoms and signs of SDPN. The NDS and NSS versions used in this study were derived from the version modified by Young et al. NDS was obtained with the examination of the ankle reflex, vibration, pin-prick, and temperature sensation cold tuning fork in the big toe.
The total maximum abnormal score on this scale was A score of 3—5 was regarded as evidence of mild neuropathic signs, 6—8 as evidence of moderate signs and a score of 9—10 was regarded as evidence of severe signs of neuropathy. The NSS was based on questioning the patients about their experiences of pain or discomfort in the legs.
The maximum symptom score on this scale was 9. A symptom score of 3—4 was regarded as mild symptoms, a score of 5—6 as moderate symptoms and a score of 7—9 as severe symptoms of neuropathy. The minimum acceptable criteria for a diagnosis of peripheral neuropathy were: moderate signs with or without symptoms, or mild signs with moderate symptoms.
Mild signs alone or with mild symptoms were not considered to be an adequate parameter for a diagnosis of peripheral neuropathy.
Global cognitive function was assessed by using the Portuguese Version of the Mini-Mental State Examination MMSE [ 11 ]. Trail Making Tests A TMT-AB TMT-B and Verbal Fluency Test VFT - Animals were also used to evaluate general aspects of cognition. Statistical analysis was performed with GraphPad InStat 3.
For non parametric variables, data are presented as median [lower limit—upper limit]. Spearman test was used for correlation analysis of nonparametric variables. One hundred patients with DM and 60 healthy individuals were invited to join the study.
Six patients in both group refused to participate. Initially, patients with T2DM were compared with the control group.
No differences were found in age, gender or years of formal education Table 1. When cognitive function was evaluated, significantly lower scores were found in the T2DM group in comparison to control group in the MMSE No differences were found in TMT-A A trend toward significance were found in TMT-B Patients with and without PDN were compared and no differences were observed in age, gender, educational level, marital status and disease duration data not shown.
Also, no differences were found between patients with and without PDN in all cognitive tests Table 2. No correlation was also found among NSS, NDS and any of the cognitive tests data not shown.
Although some mechanisms linking these diseases have already been established, several points are still controversial [ 312 ]. In particular, it remains to be determined whether cognitive impairment could have any relationship with other microvascular complications of DM, particularly DN.
In line with this, we investigated whether the presence of DPN would be associated with cognitive functioning. Different mechanisms have already been proposed for DN pathogenesis. Some of these mechanisms have already been linked to the pathogenesis of cognitive impairment, including oxidative stress, microvascular vasculopathy, inflammation, dyslipidemia, among others [ 4 — 8 ].
Although these may be considered common mechanisms for both DN and cognitive impairment, no correlation between these two complications was found in our study. Further studies are necessary to clarify this issue. There are some explanations for our findings.
First, the diagnosis of DPN was based only in clinical scales. Although these scales are widely used, it would be very interesting to compare findings from cognitive with nerve conduction tests. It should be noted that there were patients who scored less than 24 in MMSE, suggesting that individuals with dementia may have been included in the study.
This might be of great relevance, particularly because NDS and NSS have not been validated in this specific population. NDS is based on the assessment of peripheral sensitivity, which completely depends on the ability of the patient to understand what is been asked and what is been done by the examiner.
The same considerations can also be applied to NSS, which depends on the comprehension of specific questions to determine different symptoms. It is impossible to evaluate, at this moment, how cognitive impairment would influence the results of these scores i.
false-positives or false-negatives. However, it is worthy noticing that these scales have already been used in populations that included older individuals and dementia has not been evaluated in these studies 9, Second, the cognitive impairment that occurs in T2DM may have completely different mechanisms from the ones that affect peripheral nerves.
Although these complications do share some similarities as discussed abovemultiple and individual components may play an important role in determining who will develop central and who will develop peripheral nerve destruction. Third, the vast majority of patients included in this study were women.
Further studies are necessary to clarify whether the same results would also be demonstrated in men. Finally, there are other variables that could be of great relevance for the association of PDN and cognitive impairment, including Body Mass Index, Glycemic Control including hypoglycemiaand lipid profile.
Unfortunately, these variables were not accessed in this study. In summary, cognitive impairment seems to be more severe in T2DM than in non-diabetic individuals. Further studies are necessary to clarify whether these findings would also be applicable to different populations, with different stages of cognitive impairment and neuropathy.
Singh R, Kishore L, Kaur N. Diabetic peripheral neuropathy: current perspective and future directions. Pharmacol Res. Article CAS PubMed Google Scholar. Bloemer J, Bhattacharya S, Amin R, Suppiramaniam V. Impaired insulin signaling and mechanisms of memory loss.
Prog Mol Biol Transl Sci. CAS PubMed Google Scholar. Moreira RO, Campos SC, Soldera AL. Diabetes Metab Res Rev. doi: PubMed Google Scholar. Pohanka M. Curr Med Chem. Article Google Scholar. Schrag M, Mueller C, Zabel M, Crofton A, Kirsch WM, Ghribi O, et al. Neurobiol Dis.
Languren G, Montiel T, Julio-Amilpas A, Massieu L. Neuronal damage and cognitive impairment associated with hypoglycemia: An integrated view. Neurochem Int.
: Cognitive impairment in diabetic neuropathy| Does ‘Cognitive Neuropathy’ Contribute To Non-Adherence In Patients With Diabetes? | Diabetic patients frequently develop microvascular complications such as nephropathy, retinopathy, peripheral neuropathy PN , and sexual and cognitive disorders due to capillary dysfunction and metabolic disturbances [ 2 ]. Pfutzner A, Forst T, Engelbach M, et al. Email alerts Online First Alert. Centers for Medicare and Medicaid Services. Ochoa-Reparaz, J. |
| ORIGINAL RESEARCH article | Abstract Cognitive impairment CI and distal polyneuropathy are the most common neurological Cognittive of diabetes mellitus Natural immune system boosters Herbal tea remedies for blood pressure depend not only on neuropatuy severity and duration of Doabetic, but also on the presence of concomitant diseases. Table 5. Spermine protects from LPS-induced memory deficit via BDNF and TrkB activation. PN was also positively associated with the separate outcomes of MCI RRR 1. The study was conducted in compliance with the ethical standards of the responsible institution on human subjects as well as with the Helsinki Declaration. |
| Diabetic peripheral neuropathy linked to cognitive decline in type 2 diabetes | At this vein, it is well known that DNP is a chronic disease associated with long-term suffering and disability, and with significant interference in daily life It can explain the observed significant impact on mental health, quality of life and sleep in DNP patients, compared to those without DNP, as shown in several studies 16 , 17 , Regarding the results observed for cognitive function, other authors 13 report that patients with T2DM, both with and without DNP, may present cognitive impairment. In this sense, Zhang et al. A noteworthy result is the fact that the subjects with DNP performed worse in verbal fluency that those without DNP. Verbal fluency depends on the correct functioning of the prefrontal cortex, a region that could be affected by pain processing, which could explain the results observed in our study However, these data should be interpreted with caution, as they relied exclusively on the TYM measure. Additional tests evaluating these domains are recommended for future studies. Analysing the factors associated with cognitive function in the patients with DNP, those that were older and those under treatment with insulin obtained lower scores on the TYM scale more impairment. Regarding age, several studies 1 , 2 have shown an inverse relationship with cognitive functioning. Similarly, DNP and diabetes have been reported to be considerably more prevalent among older people 9 , evidence existing that patients suffering from CP and diabetes presenting worse cognitive functioning. In the case of diabetes, this impairment is related with an increase in insulin resistance, greater fluctuations of glucose and high levels of HbA1c 38 ; as for chronic pain, it is associated with the interference produced by the pain in important regions for cognitive performance such as the prefrontal cortex and the hippocampus 7. With respect to insulin treatment, some authors highlight that the patients receiving this treatment most frequently have the disease the longest and present worse metabolic control, which, as mentioned above, are factors associated with impaired cognitive function in individuals with diabetes The relation between cognitive impairment and depression found in the study has been shown in previous studies carried out in diabetic patients with peripheral neuropathy. In this line, a recently published meta-analysis 39 shows that this relationship could be partly due to psychosocial stress produced for suffering a chronic illness 4. Furthermore, the presence of pain in these patients is related to loss of functional capacity and social contacts that also increase the risk of depressive symptoms All of these factors can lead to a decrease of self-sufficiency 5 , 40 , and consequently to decrease cognitive function asreported by Calatayud et al. The relationship observed between cognitive function and level of education is in agreement with that found in other studies 40 , where a higher level of education was related with a greater cognitive reserve Moreover, it has been shown that the higher the educational level, the better the control and knowledge of the disease, and self-care practices and adherence to treatment is better, which are factors related with maintaining cognitive functioning in persons with diabetes 43 , Another result of our study, again in line with the literature, is that higher scores on the mental and physical component of quality of life are associated with better cognitive function in patients with DNP. Better physical and mental health means less limitations in performing daily activities, greater autonomy and a greater chance of the patients conducting rewarding activities, which has been shown to stimulate cognitive functioning 45 , Unexpected results were the inverse relationship between cognitive function and AHT multiple linear regression model or that found with quality of sleep binary logistic regression model. Generally, AHT is a risk factor that is often related with the presence of diabetes and cognitive impairment 5. However, other studies have reported the opposite to be true More specifically, Ruitenberg et al. Along these lines, den Heijer et al. Moreover, on the basis of taking medication for hypertension being associated with less cognitive impairment 47 , a possible hypothesis for explaining our results is that patients diagnosed with AHT take medication for it and are therefore more controlled, unlike those without a diagnosis and who logically are not under treatment for it. However, no information was included in this study about taking medication for hypertension, making it impossible to prove this hypothesis. Finally, although sleep disorders are common among persons with diabetes with DNP 16 , and other studies have shown them to be related with impaired cognitive performance 40 , this relationship was not observed in this study. One explanation could be the different instruments used in these studies, the Pittsburgh Sleep Quality Index often being used Moreover, our results are based on the Index 9, a complex index constructed using the sum of different items that comprise the dimensions in the MOS scale, where we observe inverse relationships with the TYM in the scores of these dimensions. For example, better results are obtained among subjects with impairment in the sleep disturbance and adequacy of sleep dimensions; however, among the subjects without cognitive impairment, the results on the shortness of breath dimension are better data not shown. Taking hypnotic medication was associated with a lower risk of impairment, as expected, as sleep-enhancing drugs have been shown to mitigate cognitive impairment if the kind used and the doses prescribed are controlled The frequency of taking these drugs was high among the patients with DNP, which could influence the result observed on the Index-9, although information about the type and dose was not collected in the study. As strengths, we highlight the use of validated scales that enable better information to be obtained from the population analysed. Likewise, the multi-centred design allowed us to obtain a more representative sample, although it was not possible to reach the sample size initially calculated due to the Covid pandemic, which forced us to put an end to the data collection earlier than planned. Although this is a limitation that could diminish the power of the study, the information provided by the study is still relevant. Another strength is that we have analysed the cognitive domains of the TYM separately in order to obtain more detailed information about the dimensions that encompass cognitive function, an innovative topic that has not been studied before, to our knowledge. As a limitation, it is necessary to highlight that the cross-sectional design of the study does not allow causal relationships to be established between cognitive function and the variables studied. Furthermore, although some authors recommend multiple instruments to more reliably assess the dimensions of cognitive function, we only use TYM to ensure that the assessment session did not take too long. The TYM scale has been translated, adapted and validated in Spanish in patients with chronic pain included neuropathic pain by our research group 27 , Another limitation is our specific selection of high-risk patients, which could bias the sample in favor of those with more severe mood and sleep disorders, and worse cognitive function. However, we decided to choose this group of patients because they were more likely to suffer from diabetic neuropathy and DNP, making the study more efficient. This study shows that patients with T2DM, both with and without DNP, present cognitive impairment. No greater risk was observed when the pain was more intense or according to the sensory profile of the patients. In addition, it is noteworthy that being older, treatment with insulin, obesity, a longer duration of diabetes and the presence of depression were associated with a greater risk of cognitive impairment in patients with DNP. While a higher level of education, a better mental and physical component of quality of life, a higher AHT and a poor quality of sleep were associated with a better cognitive function in patients with DNP. Identifying and controlling these factors should be an essential intervention for maintaining the cognitive function of patients with T2DM and DNP. The datasets analysed during the current study are available from the corresponding author on reasonable request. Jongsiriyanyong, S. Mild cognitive impairment in clinical practice: A review article. Article Google Scholar. Vega-Alonso, T. et al. Prevalence of cognitive impairment in Spain: The Gómez de Caso study in health sentinel networks. Neurologia 33 , — CAS PubMed Google Scholar. Other Demen. van Sloten, T. Cerebral microvascular complications of type 2 diabetes: Stroke, cognitive dysfunction, and depression. Lancet Diabetes Endocrinol. Article PubMed Google Scholar. Li, W. Prevalence, influence factors and cognitive characteristics of mild cognitive impairment in type 2 diabetes mellitus. Aging Neurosci. Google Scholar. Whitlock, E. Association between persistent pain and memory decline and dementia in a longitudinal cohort of elders. JAMA Intern. Article PubMed PubMed Central Google Scholar. Bell, T. Persistence of pain and cognitive impairment in older adults. Achterberga, W. Pain in dementia. Pain 1 , e Shillo, P. Painful and painless diabetic neuropathies: What is the difference?. Rosenberger, D. Challenges of neuropathic pain: Focus on diabetic neuropathy. Neural Transm. Pop-Busui, R. Diabetic neuropathy: A position statement by the American diabetes association. Diabetes Care 40 , — Article CAS PubMed Google Scholar. Sloan, G. A new look at painful diabetic neuropathy. Diabetes Res. Elsharkawy, R. Peripheral polyneuropathy and cognitive impairment in Type II diabetes mellitus. Naranjo, C. Relationship between diabetic neuropathic pain and comorbidity. Their impact on pain intensity, diabetes complications and quality of life in patients with type-2 diabetes mellitus. Selvarajah, D. Magnetic resonance neuroimaging study of brain structural differences in diabetic peripheral neuropathy. Diabetes Care 37 , — Anxiety, depression and sleep disorders in patients with diabetic neuropathic pain: A systematic review. Expert Rev. Kioskli, K. Psychosocial factors in painful diabetic neuropathy: A systematic review of treatment trials and survey studies. Pain Med. US 20 , — Bobo, W. Association of depression and anxiety with the accumulation of chronic conditions. JAMA Netw. Open 5 , e Haack, M. Sleep deficiency and chronic pain: Potential underlying mechanisms and clinical implications. Neuropsychopharmacology 45 , — Orgeta, V. Psychological treatments for depression and anxiety in dementia and mild cognitive impairment. Cochrane Datab. American Diabetes Association. Classification and diagnosis of diabetes: Standards of medical care in diabetes Diabetes Care 44 , S15—S33 Association, A. Classification and diagnosis of diabetes. Diabetes Care 39 , S13—S22 Article CAS Google Scholar. Zhang, Q. Easier operation and similar power of 10 g monofilament test for screening diabetic peripheral neuropathy. Article ADS PubMed PubMed Central Google Scholar. Perez, C. Validity and reliability of the Spanish version of the DN4 Douleur Neuropathique 4 questions questionnaire for differential diagnosis of pain syndromes associated to a neuropathic or somatic component. Health Qual. Life Outcomes 5 , 1—10 Brown, J. BMJ , — Test Your Memory TYM test : Diagnostic evaluation of patients with non-Alzheimer dementias. Ojeda, B. Assessing the construct validity and internal reliability of the screening tool test your memory in patients with chronic pain. PLoS ONE 11 , 1—16 Traducción y adaptación al castellano del Cuestionario de Detección de Trastorno Cognitivo Leve. The contributors of emotional distress in painful diabetic neuropathy. Herrero, M. A validation study of the hospital anxiety and depression scale HADS in a Spanish population. Psychiatry 25 , — Quintana, J. Evaluation of the psychometric characteristics of the Spanish version of the Hospital Anxiety and Depression Scale. Acta Psychiatr. Viala-Danten, M. Evaluation of the reliability and validity of the Medical Outcomes Study sleep scale in patients with painful diabetic peripheral neuropathy during an international clinical trial. Life Outcomes 6 , 1—12 Schmidt, S. Normas de referencia para el Cuestionario de Salud SF versión 2 basadas en población general de Cataluña. Article ADS Google Scholar. Villoria, J. Psychometric validation of the neuropathic pain symptom inventory for its use in Spanish. Pain Symptom. Manag 42 , — Gylfadottir, S. Diabetic polyneuropathy and pain, prevalence, and patient characteristics: A cross-sectional questionnaire study of 5, patients with recently diagnosed type 2 diabetes. Pain , — Zhang, X. Perspectives of glycemic variability in diabetic neuropathy: A comprehensive review. Chou, P. Reduced frontal activity during a verbal fluency test in fibromyalgia: A near-infrared spectroscopy study. Sharma, G. Cognitive impairments in type 2 diabetes, risk factors and preventive strategies. Basic Clin. Article ADS CAS Google Scholar. Palomo-Osuna, J. Cognitive function in diabetic persons with peripheral neuropathy: A systematic review and meta-analysis. Factors influencing cognitive impairment in neuropathic and musculoskeletal pain and fibromyalgia. Calatayud, E. Cognitive differences in the older adults living in the general community: Gender and mental occupational state study. Public Health 18 , 1—12 Moran, C. Type 2 diabetes mellitus, brain atrophy, and cognitive decline. Neurology 92 , E—E Article CAS PubMed PubMed Central Google Scholar. Almigbal, T. Association of health literacy and self-management practices and psychological factor among patients with type 2 diabetes mellitus in Saudi Arabia. Saudi Med. RobatSarpooshi, D. The relationship between health literacy level and self-care behaviors in patients with diabetes. Patient Relat. Outcome Meas. Mandolesi, L. Effects of physical exercise on cognitive functioning and wellbeing: Biological and psychological benefits. Bai, A. Effects of physical activity on cognitive function among patients with diabetes in China: A nationally longitudinal study. BMC Public Health 21 , 1 Iadecola, C. Neurovascular and cognitive dysfunction in hypertension: Epidemiology, pathobiology, and treatment. Ruitenberg, A. Blood pressure and risk of dementia: Results from the Rotterdam study and the Gothenburg H study. den Heijer, T. Association between blood pressure levels over time and brain atrophy in the elderly. Aging 24 , — Buysse-Charles, F. The Pittsburgh sleep quality index: A new instrument for psychiatric practice and research. Psychiatry Res. Burke, S. Mild cognitive impairment: Associations with sleep disturbance, apolipoprotein e4, and sleep medications. Sleep Med. Download references. Observatory of Pain, Grünenthal Foundation-University of Cadiz, , Cádiz, Spain. Biomedical Research and Innovation Institute of Cadiz INiBICA , , Cádiz, Spain. Preventive Medicine and Public Health Area, University of Cádiz, , Cádiz, Spain. Department of Statistics and Operational Research, University of Cádiz, , Puerto Real, Spain. University Hospital Puerta del Mar, , Cádiz, Spain. You can also search for this author in PubMed Google Scholar. supervised the study. and M. led the writing. and A. Physiol Rev. Lindsay ZA, Chadrasekaran K, Kwan JY, Russell JW. Diabetes and Cognitive Impairment. Curr Diab Rep. Launer LJ, Miller ME, Williamson JD, et al. Effects of intensive glucose lowering on brain structure and function in people with type 2 diabetes ACCORD MIND : a randomised open-label substudy. Lancet Neurol. Erus G, Battapady H, Zhang T, et al. Spatial patterns of structural brain changes in type 2 diabetic patients and their longitudinal progression with intensive control of blood glucose. Epub Oct Boulton AJM. Diabetic neuropathy and foot complications. Handb Clin Neurol. Lobmann R. Diabetic foot syndrome. Internist Berl. Volmer-Thole M, Lobmann R. Neuropathy and Diabetic Foot Syndrome. Int J Mol Sci. Malik RA, Tesfaye S, Newrick PG, et al. Sural nerve pathology in diabetic patients with minimal but progressive neuropathy. Epub Feb Pfutzner A, Forst T, Engelbach M, et al. The influence of isolated small nerve fibre dysfunction on microvascular control in patients with diabetes mellitus. Diabet Med. Cameron NE, Eaton SE, Cotter MA, Tesfaye S. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy. Brown MR, Dyck PJ, McClearn GE, et al. Central and peripheral nervous system complications. Dyck PJ, Windebank AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: New insights into pathophysiology and treatment. Muscle Nerve. Pop-Busui R, Boulton AJ, Feldman EL, et al. Diabetic Neuropathy: A Position Statement by the American Diabetes Association. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Capodanno D, Angiolillo DJ. Aspirin for Primary Cardiovascular Risk Prevention and Beyond in Diabetes Mellitus. American Diabetes Association. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes Boer IH, Bakris G, Cannon CP. Gromova OA, Torshin IYu, Kalacheva AG, et al. The triple synergy of ethylmethylhydroxypyridine succinate, magnesium, and vitamin B6: Molecular mechanisms. In Russ. Ziegler D, Ametov A, Barinov A, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial. Strokov IA, Akhmetzhanova LT, Solokha OA. Effectiveness of treatment of diabetic polyneu ropathy with alpha-lipoic acid tablets. Trudnyi patsient. Ruhnau KJ, Meissner HP, Finn JR, et al. Effects of 3-week oral treatment with the antioxidant thioctic acid alpha-lipoic acid in symptomatic diabetic polyneuropathy. Ametov AS, Barinov A, Dyck PJ, et al. The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid: the SYDNEY trial. Ziegler D, Nowak H, Kempler P, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis. Strokov IA, Zakharov VV, Strokov KI. Diabetic encephalopathy. Starchina YuA, Zakharov VV. Neurological complications of diabetes mellitus. Effektivnaya farmakoterapiya. Kosivtsova O. Cognitive impairment and distal polyneuropathy in a patient with diabetes mellitus in neurological outpatient practice. Neurology, Neuropsychiatry, Psychosomatics. Kosivtsova Department of Nervous System Diseases and Neurosurgery, N. Sklifosofsky Institute of Clinical Medicine, A. Kozhevnikov Clinic of Nervous System Diseases, I. Sechenov First Moscow State Medical University Sechenov University , Ministry of Health of Russia Russian Federation. Platov City Polyclinic Forty-Six, Moscow Healthcare Department Russian Federation. Kochetov City Polyclinic Forty-Six, Moscow Healthcare Department Russian Federation. The web-site of this journal uses cookies to optimize its performance and design as well as special service to collect and analyze data about pages visitors. By continuing to browse this web-site you agree to use cookies and the above service. More about cookies. Neurology, Neuropsychiatry, Psychosomatics Nevrologiâ, nejropsihiatriâ, psihosomatika. eng рус. ISSN Print ISSN Online. |
| Related Content | Microbiota-gut-brain axis and cognitive function. Neurovascular and cognitive dysfunction in hypertension: Epidemiology, pathobiology, and treatment. Correspondence to Xia Zhang. Neuropathy and Diabetic Foot Syndrome. Author Guidelines. |
| Of the study cohort, Statement of Ethics. Patients were excluded from the study that did not meet the inclusion criteria, those presenting any kind of neurodegenerative disease with cognitive impairment, those that were unable to complete the scales due to a physical limitation, and when neuropathy was ruled out by the foot examination. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Article CAS Google Scholar Chou, P. Дисциркуляторная энцефалопатия и сосудистые когнитивные расстройства. |
Cognitive impairment in diabetic neuropathy -
To dissect the common pathogenic mechanisms of both, further longitudinal clinical and morphological studies including T1DM patients with both cognitive and DPN are needed. The current study has some limitations.
We cannot determine causality because of the cross-sectional design. The sample size was relatively small. HbA1c levels were only determined once, so the relationship between continued blood sugar levels and cognitive dysfunction has not been discussed.
There were seldom DKA or severe hypoglycemia attacks for the subjects, so we have not considered those factors into logistic analysis and the clinical significance of both hypo- and hyperglycemia on cognitive function could not be figured out.
Therefore, it is cautioned that our findings should be supported by future work in larger prospective longitudinal studies. In conclusion, this study has identified cognitive impairments in an adult Chinese population with T1DM and connection between cognitive dysfunction and DPN, which provides new insights on the pathogenic mechanisms of both cognitive impairment and DPN of T1DM patients.
However, the definitive pathogenesis and alteration of cognitive impairment requires larger, prospective, longitudinal studies and appropriate, strict enrollment of subjects.
Moheet A, Mangia S, Seaquist ER. Impact of diabetes on cognitive function and brain structure. Ann N Y Acad Sci. Article Google Scholar. Ohmann S, Popow C, Rami B, Konig M, Blaas S, Fliri C, Schober E.
Cognitive functions and glycemic control in children and adolescents with type 1 diabetes. Psychol Med. Article CAS Google Scholar. Li W, Huang E, Gao S. Type 1 diabetes mellitus and cognitive impairments: a systematic review.
J Alzheimers Dis. Deli G, Bosnyak E, Pusch G, Komoly S, Feher G. Diabetic neuropathies: diagnosis and management. Selvarajah D, Wilkinson ID, Davies J, Gandhi R, Tesfaye S. Central nervous system involvement in diabetic neuropathy.
Cur Diab Rep. Lee MC, Tracey I. Imaging pain: a potent means for investigating pain mechanisms in patients. Br J Anaesth. Gubitosi-Klug RA. Diabetes Care. Zhou Y, Fang R, Liu LH, Chen SD, Tang HD.
Clinical characteristics for the relationship between type-2 diabetes mellitus and cognitive impairment: a cross-sectional study. Aging Dis. Zhang X, Fang C, Li X, Cao YJ, Zhang QL, Zhang HH, Huang Y, Hu J, Liu CF.
Clinical characteristics and risk factors of diabetic peripheral neuropathy of type 1 diabetes mellitus patients. Diabetes Res Clin Pract. Folstein MF, Folstein SE, McHugh PR. A practical method for grading the cognitive state of patients for the clinician.
J Psychiatr Res. Nasreddine ZS, Phillips NA, Bedirian V, Charbonneau S, Whitehead V, Collin I, Cummings JL, Chertkow H. The Montreal cognitive assessment, MoCA: a brief screening tool for mild cognitive impairment.
J Am Geriatr Soc. Tonoli C, Heyman E, Roelands B, Pattyn N, Buyse L, Piacentini MF, Berthoin S, Meeusen R. Type 1 diabetes-associated cognitive decline: a meta-analysis and update of the current literature.
J Diabetes. Nunley KA, Rosano C, Ryan CM, Jennings JR, Aizenstein HJ, Zgibor JC, Costacou T, Boudreau RM, Miller R, Orchard TJ, Saxton JA. Clinically relevant cognitive impairment in middle-aged adults with childhood-onset type 1 diabetes.
Morys JM, Kozera GM, Neubauer-Geryk J, Kruszewski P, Wolnik B, Nyka WM, Bieniaszewski L. Statin use and cognitive impairment in patients with type 1 diabetes: an observational study.
Clin Neuropharmacol. Wilkinson ID, Selvarajah D, Greig M, Shillo P, Boland E, Gandhi R, Tesfaye S. Magnetic resonance imaging of the central nervous system in diabetic neuropathy. Curr Diab Rep. Greig M, Tesfaye S, Selvarajah D, Wilkinson ID.
Insights into the pathogenesis and treatment of painful diabetic neuropathy. Handb Clin Neurol. Selvarajah D, Wilkinson ID, Emery CJ, Shaw PJ, Griffiths PD, Gandhi R, Tesfaye S.
Thalamic neuronal dysfunction and chronic sensorimotor distal symmetrical polyneuropathy in patients with type 1 diabetes mellitus.
Selvarajah D, Wilkinson ID, Gandhi R, Griffiths PD, Tesfaye S. Microvascular perfusion abnormalities of the thalamus in painful but not painless diabetic polyneuropathy: a clue to the pathogenesis of pain in type 1 diabetes. Northam EA, Rankins D, Lin A, Wellard RM, Pell GS, Finch SJ, Werther GA, Cameron FJ.
Central nervous system function in youth with type 1 diabetes 12 years after disease onset. Selvarajah D, Wilkinson ID, Maxwell M, Davies J, Sankar A, Boland E, Gandhi R, Tracey I, Tesfaye S.
Magnetic resonance neuroimaging study of brain structural differences in diabetic peripheral neuropathy. Nunley KA, Ryan CM, Orchard TJ, Aizenstein HJ, Jennings JR, Ryan J, Zgibor JC, Boudreau RM, Costacou T, Maynard JD, Miller RG, Rosano C.
White matter hyperintensities in middle-aged adults with childhood-onset type 1 diabetes. Zilliox LA, Chadrasekaran K, Kwan JY, Russell JW. Diabetes and cognitive impairment. Ryan CM, Williams TM, Orchard TJ, Finegold DN.
Psychomotor slowing is associated with distal symmetrical polyneuropathy in adults with diabetes mellitus. Download references. We are deeply appreciative of the participants in this study and thank all staffs for their support and assiatance.
This study was supported by grants from the National Natural Science Foundation of China , , This was also partly supported by the preponderant clinic discipline group project funding of the Second Affiliated Hospital of Soochow University XKQ The funder of and was Xin Ding who was the first author, analyzing and interpreting the patient data regarding the cognitive functioning and nerve conduction velocity NCV results, and writing part of the manuscript.
The funder of was Yong-Jun Cao who participated in the design of the study and monitoring its implement. The funder of XKQ was responsible for publication charges. Department of Endocrinology, the Second Affiliated Hospital of Soochow University, Suzhou, , China. Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, Sanxiang Road, Suzhou, , China.
You can also search for this author in PubMed Google Scholar. DX analyzed and interpreted the patient data regarding the cognitive functioning and nerve conduction velocity NCV results, and was a major contributor in writing the manuscript. FC was responsible for diagnosing, enrolling patients and collecting their basic data, and was a contributor in writing the manuscript.
LX and ZQL performed the NCV tests and cognition evaluation. CYJ and PJ participated in the design of the study and monitoring its implement. HY was responsible for the statistical analysis.
ZX was responsible for the design of the study, organizing the implement of the trial and revising the manuscript. All authors read and approved the final manuscript.
Correspondence to Xia Zhang. Different mechanisms have already been proposed for DN pathogenesis. Some of these mechanisms have already been linked to the pathogenesis of cognitive impairment, including oxidative stress, microvascular vasculopathy, inflammation, dyslipidemia, among others [ 4 — 8 ].
Although these may be considered common mechanisms for both DN and cognitive impairment, no correlation between these two complications was found in our study. Further studies are necessary to clarify this issue.
There are some explanations for our findings. First, the diagnosis of DPN was based only in clinical scales. Although these scales are widely used, it would be very interesting to compare findings from cognitive with nerve conduction tests. It should be noted that there were patients who scored less than 24 in MMSE, suggesting that individuals with dementia may have been included in the study.
This might be of great relevance, particularly because NDS and NSS have not been validated in this specific population. NDS is based on the assessment of peripheral sensitivity, which completely depends on the ability of the patient to understand what is been asked and what is been done by the examiner.
The same considerations can also be applied to NSS, which depends on the comprehension of specific questions to determine different symptoms. It is impossible to evaluate, at this moment, how cognitive impairment would influence the results of these scores i.
false-positives or false-negatives. However, it is worthy noticing that these scales have already been used in populations that included older individuals and dementia has not been evaluated in these studies 9, Second, the cognitive impairment that occurs in T2DM may have completely different mechanisms from the ones that affect peripheral nerves.
Although these complications do share some similarities as discussed above , multiple and individual components may play an important role in determining who will develop central and who will develop peripheral nerve destruction. Third, the vast majority of patients included in this study were women.
Further studies are necessary to clarify whether the same results would also be demonstrated in men. Finally, there are other variables that could be of great relevance for the association of PDN and cognitive impairment, including Body Mass Index, Glycemic Control including hypoglycemia , and lipid profile.
Unfortunately, these variables were not accessed in this study. In summary, cognitive impairment seems to be more severe in T2DM than in non-diabetic individuals. Further studies are necessary to clarify whether these findings would also be applicable to different populations, with different stages of cognitive impairment and neuropathy.
Singh R, Kishore L, Kaur N. Diabetic peripheral neuropathy: current perspective and future directions. Pharmacol Res. Article CAS PubMed Google Scholar. Bloemer J, Bhattacharya S, Amin R, Suppiramaniam V. Impaired insulin signaling and mechanisms of memory loss.
Prog Mol Biol Transl Sci. CAS PubMed Google Scholar. Moreira RO, Campos SC, Soldera AL. Diabetes Metab Res Rev. doi: PubMed Google Scholar. Pohanka M. Curr Med Chem. Article Google Scholar. Schrag M, Mueller C, Zabel M, Crofton A, Kirsch WM, Ghribi O, et al.
Neurobiol Dis. Languren G, Montiel T, Julio-Amilpas A, Massieu L. Neuronal damage and cognitive impairment associated with hypoglycemia: An integrated view. Neurochem Int. Umegaki H, Kawamura T, Umemura T, Kawano N. Factors associated with cognitive decline in older adults with type 2 diabetes mellitus during a 6-year observation.
Geriatr Gerontol Int. Article PubMed Google Scholar. Imamine R, Kawamura T, Umemura T, Umegaki H, Kawano N, Hotta M, et al. Does cerebral small vessel disease predict future decline of cognitive function in elderly people with type 2 diabetes?
Diabetes Res Clin Pract. Moreira RO, Castro AP, Papelbaum M, Appolinario JC, Ellinger VC, Coutinho WF, et al. Translation into Portuguese and assessment of the reliability of a scale for the diagnosis of diabetic distal polyneuropathy. Arq Bras Endocrinol Metabol.
Young MJ, Boulton AJ, MacLeod AF, Williams DR, Sonksen PH. A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population.
Lourenço RA, Veras RP. Mini-Mental State Examination: psychometric characteristics in elderly outpatients. Rev Saude Publica. Lindsay ZA, Chadrasekaran K, Kwan JY, Russell JW. Diabetes and Cognitive Impairment.
Curr Diab Rep. Launer LJ, Miller ME, Williamson JD, et al. Effects of intensive glucose lowering on brain structure and function in people with type 2 diabetes ACCORD MIND : a randomised open-label substudy. Lancet Neurol. Erus G, Battapady H, Zhang T, et al.
Spatial patterns of structural brain changes in type 2 diabetic patients and their longitudinal progression with intensive control of blood glucose. Epub Oct Boulton AJM.
Diabetic neuropathy and foot complications. Handb Clin Neurol. Lobmann R. Diabetic foot syndrome. Internist Berl. Volmer-Thole M, Lobmann R. Neuropathy and Diabetic Foot Syndrome. Int J Mol Sci. Malik RA, Tesfaye S, Newrick PG, et al.
Sural nerve pathology in diabetic patients with minimal but progressive neuropathy. Epub Feb Pfutzner A, Forst T, Engelbach M, et al. The influence of isolated small nerve fibre dysfunction on microvascular control in patients with diabetes mellitus.
Diabet Med. Cameron NE, Eaton SE, Cotter MA, Tesfaye S. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy.
Brown MR, Dyck PJ, McClearn GE, et al. Central and peripheral nervous system complications. Dyck PJ, Windebank AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: New insights into pathophysiology and treatment.
Muscle Nerve. Pop-Busui R, Boulton AJ, Feldman EL, et al. Diabetic Neuropathy: A Position Statement by the American Diabetes Association. Antithrombotic Trialists' Collaboration.
Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Capodanno D, Angiolillo DJ. Aspirin for Primary Cardiovascular Risk Prevention and Beyond in Diabetes Mellitus.
American Diabetes Association. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes Boer IH, Bakris G, Cannon CP. Gromova OA, Torshin IYu, Kalacheva AG, et al. The triple synergy of ethylmethylhydroxypyridine succinate, magnesium, and vitamin B6: Molecular mechanisms.
In Russ. Ziegler D, Ametov A, Barinov A, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial. Strokov IA, Akhmetzhanova LT, Solokha OA. Effectiveness of treatment of diabetic polyneu ropathy with alpha-lipoic acid tablets.
Trudnyi patsient. Ruhnau KJ, Meissner HP, Finn JR, et al. Effects of 3-week oral treatment with the antioxidant thioctic acid alpha-lipoic acid in symptomatic diabetic polyneuropathy.
Caitlin W. HicksHerbal tea remedies for blood pressure WangImpairmejt L. Schneider neuropathh, Michelle C. Blood circulation massageRebecca F. GottesmanKunihiro MatsushitaJosef CoreshB. Gwen WindhamElizabeth Selvin; Associations of Peripheral Neuropathy Defined by Monofilament Insensitivity with Mild Cognitive Impairment and Dementia in Older Adults. Dement Geriatr Cogn Disord 1 June ; 51 2 : —
Sie irren sich. Ich kann die Position verteidigen. Schreiben Sie mir in PM, wir werden reden.
Sie sind nicht recht. Geben Sie wir werden es besprechen. Schreiben Sie mir in PM, wir werden umgehen.
Ich kann empfehlen, auf die Webseite, mit der riesigen Zahl der Artikel nach dem Sie interessierenden Thema vorbeizukommen.
Sie sind nicht recht. Schreiben Sie mir in PM, wir werden reden.