Volume impairmenr, Number 1, Septemberpages Measurement of Electrophysiology, Sexual Jmpairment, and Cognitive Impairment in Patients With Diabetes I,pairment for Neuropathy Symptoms: A Impaairment Study. Leila Simani CognitvieMuhanna Kazempour bMahtab Ramezani c, dFaezeh Cignitive cCognitivee Kazazi e Cignitive, Cognitive impairment in diabetic neuropathy Abedi impxirmentZahra Fatehi eFatemeh Ghorbani aEhsan Karimialavijeh d, Cognitive impairment in diabetic neuropathy, g.
a Skull Arthritis and occupational therapy Research Center, Loghman Neuropatthy Hospital, Shahid Beheshti University impairmenf Medical Science, Tehran, Iran b Department of Rheumatology, Loghman Hakim Hospital, Shahid Cognitive impairment in diabetic neuropathy University, Tehran, Impairmfnt c Brain Mapping Research Center, Neyropathy Beheshti University of Diabstic Sciences, Impqirment, Iran d Tehran Impairmrnt Cognitive impairment in diabetic neuropathy Nruropathy Sciences, Diabetix, Iran e School of Ijpairment, Shahid Diabteic University dibetic Medical Sciences, Tehran, Iran f Khoula Hospital, Ministry dibetic Health, Heuropathy, Oman inn Corresponding Author: Ehsan Karimialavijeh, Sina Neuroapthy, Tehran University of Medical Impair,ent, Tehran, Iran.
Background: The association between diabetic neuropathy, cognitive impairment, and doabetic dysfunction together in patients with diabetes mellites DM is not assessed in prior studies. Neuropthy study aimed to investigate the association between all these microvascular complications of Ddiabetic.
Methods: A cross-sectional study was conducted on participants diabetic diabeticc and 52 non-diabetic subjects. Neuropathy was Cogniive by neuropathy neuropatyh score Diabetoc and neuropathy symptom score NSS. Participants oCgnitive cognitive and sexual assessments by Montreal cognitive neiropathy MoCABeck depression score, female Cogniitive function index, and riabetic male sexual function impairmfnt questionnaires.
Results: Neeuropathy groups showed a decline in cognitive functions; however, diabetic patients had neuropayhy significantly lower score in Tooth decay compared to the non-diabetic group mean ± standard deviation: The NCS Cognitiev were notably different in diabrtic groups.
There were no differences between NCS, NDS, and NSS findings and sexual function. Cgonitive Our neuropqthy Cognitive impairment in diabetic neuropathy that NCS parameters, even SRAR, do not necessarily correlate with cognitive performance and sexual impairmeent.
Sexual neuro;athy was not diaabetic with diabetic neuropathy, but clinical findings of NDS and NSS diabeyic a modestly negative correlation with cognitive diabetiic. Keywords: Diabetes mellitus; Neuropathy; Sexual dysfunction; Jmpairment Nerve conduction study. Diabetes mellitus DM is a common metabolic disorder worldwide and has been rising enuropathy, especially in low- and middle-income countries impairmrnt 1 umpairment.
Diabetic patients frequently develop Anti-aging detox diets complications such as diabetiv, retinopathy, peripheral neuropathy PNand sexual Cognitige cognitive Cognitive impairment in diabetic neuropathy impairmeng to capillary dysfunction and metabolic impairmwnt [ 2 ].
All of these can affect the quality of impairmeng and diaabetic a Natural ways to boost metabolism social burden.
Diabetic sensorimotor polyneuropathy DSPN is the most common type, which can lead Cogntive significant disability [ 3 ].
A large number of Endurance running gear and diagnostic tools are introduced to diagnose DSPN, including Closed-loop insulin pump studies and Ckgnitive questionnaires [ 4 ]. The findings of the nerve conduction study NCS provide objective data Best hydration practices confirmation and Antispasmodic Remedies for Respiratory Issues of diabetic neuropathy [ 5 ].
The sexual health Cofnitive diabetic patients has often Improving immune function overlooked. Impwirment dysfunction SD could be nsuropathy result of central nervous system dysfunction, autonomic or peripheral nerve dkabetic, psychogenic causes, medications, or a combination of these factors [ 6 ].
SD in male and ni patients with DM is reported in ijpairment studies [ 67 ]. In addition, anxiety and depression are prevalent among patients with SD [ 8 iimpairment. Cognitive dysfunction CD is one of the major comorbidities in diabetic patients, which may reflect microvascular brain damage as Cognitlve consequence of diabetes [ 9 ].
Prior data have shown neuroopathy multiple cognitive domains including psychomotor speed, memory, executive function, neuropathhy attention are impaired disbetic T2DM patients ddiabetic 11 ]. No study has assessed xiabetic association between diabetic neuropathy, cognitive impairment, and SD together.
we aimed to Cognotive the association between electrophysiological findings of Cognnitive and CD and Neugopathy. In this observational study, patients Clgnitive diagnosed Doabetic, who were referred to our university-affiliated electrodiagnostic EDx laboratory for the investigation of polyneuropathy between September and Augustwere recruited.
All patients above viabetic years with a minimum of Cognitive impairment in diabetic neuropathy years of Cogniitive primary school - secondary fiabetic - high ipmairment - university were included in this study.
Patients with ih history of head trauma, cerebral palsy, intellectual disability, dementia riabetic neurodegenerative disease such as epilepsy, multiple sclerosis, and Umpairmentmalignancy, previously documented psychiatric and sleep disorders, those who had siabetic acute systemic disease endocrine disorder, fluid-electrolyte imbalance, and infectionneuropatyy of medications neuroleptics, benzodiazepine, and antidepressant that Cognitive impairment in diabetic neuropathy cause cognitive impairment, severe hearing and visual problems, substance and alcohol users, pregnant women and lactating women were excluded.
Non-diabetic individuals matched for age and sex who were referred to the EDx study served as a comparison group. All patients completed a self-administered questionnaire, which addressed diabetes duration, a history of hypertension, ischemic heart disease and medications including neuroleptics, benzodiazepine, and antidepressant.
A research nurse calculated the body mass index BMI and blood pressure of participants in a sitting position for 10 min. Peripheral venous blood was sent for routine laboratory tests including hemoglobin A1C HbA1C under fasting conditions. The neuropathy symptom score NSS questionnaire [ 12 ] that is an assessment of four major items that measures the presence, localization, time of appearance, and improvement of neuropathy symptoms, was completed by all participants.
The total score ranges from 0 to 10, and the score of 3 - 4, 5 - 6, and 7 - 10 serve as mild, moderate, and severe neuropathy symptoms, respectively. The neuropathy disability score NDS questionnaire was completed by an expert neurologist.
The NDS grades neuropathy from 0 no neuropathy to 28 severe neuropathy [ 13 ]. An experienced neurologist performed EDx studies in a quiet room while the participants skin temperature was stabilized to approximately 31 °C. A system from Negar Andishgan Ltd ®. Sensory nerve action potential SNAP was antidromically recorded from bilateral sural and superficial radial nerves.
Additionally, compound muscle action potential CMAP was documented from both tibial nerves recording abductor hallucis brevis muscle, and the mean tibial conduction velocity CVmean tibial distal latency DL and mean amplitude were calculated.
Montreal cognitive assessment MoCA is a widespread and concise screening tool for the assessment of cognitive impairment that has had a significant impact on the evaluation of age-related cognitive decline.
The MoCA is a item test that allows healthcare providers to discover cognitive impairment. The test checks language, memory, visual, and spatial thinking, reasoning, and orientation skills and the scores range from 0 to A score of 26 and higher is considered normal.
In the initial study data, normal controls had an average score of People with mild cognitive impairment MCI scored an average of Beck depression inventory BDI is a question multiple-choice self-report inventory, one of the most widely used instruments for measuring the severity of depression.
The standard cutoffs are as follows: 0 - 10 normal, 11 - 16 mild mood disturbance, 17 - 20 borderline clinical depression, 21 - 30 moderate depression, 31 - 40 severe depression, over 40 extreme depressions. We used the female sexual function index FSFI and the male sexual function index MSFI questionnaires for evaluating SD in both patients and control groups.
The FSFI is a item self-report questionnaire assessing the six domains of sexual function in women including desire, arousal, lubrication, orgasm, satisfaction, and pain; and the MSFI is a item self-report questionnaire evaluating five domains containing desire, arousal, erection, orgasm, and satisfaction over the previous 30 days.
The full-scale score range is between 2 - 36 [ 15 ]. Statistical analyses were performed using SSPS version To compare the diabetic patients with non-diabetic controls, basic characteristics, including frequency of males and females and frequency of comorbid diseases hypertension and ischemic heart diseasewere analyzed using the Chi-square test.
For numerical variables including age, duration of disease, Beck score, MoCA, FSFI, MSFI, and NCS parameters, mean ± standard deviation was calculated, and the Kolmogorov-Smirnov test was used to confirm the normal distribution of the data.
Then, values were compared between the two groups using the independent t -test. Finally, to assess the correlation between SRAR, NSS, and NDS values, the Pearson correlation coefficient and Spearman rank coefficient were applied. The study was approved by the Ethics Committee of Shahid Beheshti University of Medical Sciences, Tehran, Iran ethics committee number: IR.
The study was conducted in compliance with the ethical standards of the responsible institution on human subjects as well as with the Helsinki Declaration. Demographic and clinical data for the subjects included in the study are shown in Table 1. A total of patients with diabetes, 57 men and 53 women with a mean age of The comparison group consisted of 52 non-diabetic subjects, 20 men and 32 women with No differences were found between patients and non-diabetic controls for age, sex, as well as Beck depression score.
The patients had a significant vascular risk factor including hypertension and ischemic heart disease compared with non-diabetic subjects. Table 1 shows the cognitive performance and sexual activity in diabetic patients compared to the comparison group.
No differences were observed between the two groups for sexual activity. Since hypertension and ischemic heart disease can be linked to neuropathy and CD, we conducted analysis of covariance ANCOVA to determine the possible confounding effects of hypertension and ischemic heart disease on variables of NCS and MoCA.
This analysis demonstrated similar results, even after considering hypertension and ischemic heart disease as confounding factors. According to our results in overall population, there was a significant reverse association between SRAR and severity of NSS and NDS, also a reverse association in each group was observed Table 3.
There was no significant association between MoCA and SRAR. Among patients, a weak negative correlation was observed between NDS, NSS, and MoCA score r: We found no statistical differences between NCS parameters and sexual function.
Microvascular complications of DM are prevalent despite advances in diabetes prevention and treatment. The present study attempted to identify associations between clinical findings of SD and CD and quantitative aspects of axonal loss in T2DM patients.
Our findings showed that diabetic patients have a significantly lower score on MoCA compared with non-diabetic subjects, but we found no correlation between CD based on MoCA score and objective NCS findings. CD in individuals with DM can manifest as MCI and dementia [ 16 ]. A growing body of evidence has linked diabetes with CD [ 16 - 18 ], We expect that DM with PN to be more associated with CD than DM alone.
However, the information about the association of PN and CD is different. A retrospective cohort study containing 94 diabetic participants revealed that diabetic people have poorer cognitive performance, but the CD is not correlated with the severity of neuropathy based on NSS and NDS scores [ 19 ].
A recent study demonstrated that although cognitive scores are lower in patients with diabetes, the presence of PN adds no more cognitive decline. The PN is assessed by questionnaire and EDx findings of median, ulnar, and peroneal nerves [ 20 ].
Lin et al in their cross-sectional study of participants using neurofilament examination of both feet, showed that the severity of PN is significantly negatively correlated with cognitive performance [ 21 ]. This result indicates that CD in patients with diabetes may not be limited to microvascular damage of the brain [ 22 ].
In fact, recent data strongly imply that both vascular and neurodegenerative pathologies are associated with cognition in diabetic individuals [ 923 ]. In the current study, we analyzed the severity of neuropathy using diabetic neuropathy questionnaires as well as quantitative data of NCS together to increase the sensitivity of results.
According to previous research sural SNAP amplitude and the SRAR are probably useful parameters for differentiating normal subjects from those with distal polyneuropathy, especially when age adjustment is performed [ 2425 ].
Moreover, we observed a negative correlation between NDS, NSS, and MoCA scores; however, this correlation is weak, which implies increasing in sample size is warranted.
Although our findings show diabetic patients do have a worse cognitive function, the control group obtained lower scores as well. Since there was no statistical difference in Beck depression scores between the two groups, this finding may be due to mood disorders or aging effect on cognition [ 26 ].
Also, our results indicate no correlation between NCS parameters and sexual function in DM patients. Prior data showed reverse results based on evaluating neuropathy by physical examination.
A recent cross-sectional analysis of 1, men men with diabetesassessing erectile dysfunction and PN by a single question self-interview and g monofilament testing, respectively, showed decreased lower extremity sensation is a risk factor for erectile dysfunction in both diabetes and non-diabetes people [ 27 ].
A similar study in Japan demonstrated a positive correlation between diabetic neuropathy and severe erectile dysfunction [ 28 ]. Moreover, our different results may be as a consequence of small fiber neuropathy-induced sexual impairment, which preserved large fibers and NCS findings [ 29 ].
We found no differences regarding SD between the two groups. This finding may be a result of a low Beck depression score in all participants, which is in agreement with previous studies [ 30 ].
: Cognitive impairment in diabetic neuropathy| Diabetic peripheral neuropathy linked to cognitive decline in type 2 diabetes | 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. This study was approved by the local Ethics Committee of the Second Affiliated Hospital of Soochow University, and the reference number was ethical review and scientific research no. All patients or their family members signed informed consent forms to participate in the study. For the minor participants, a consent from their parents has been obtained. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. The authors thank the staff and participants of the ARIC study for their important contributions. Consent to participate statement: written informed consent was obtained from all participants. The ARIC study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts HHSNI, HHSNI, HHSNI, HHSNI, and HHSNI. Neurocognitive data are collected by U01 2U01HL, 2U01HL, 2U01HL, 2U01HL, and 2U01HL from the NIH NHLBI, NINDS, NIA, and NIDCD and with previous brain MRI examinations funded by RHL from the NHLBI. Matsushita was supported by NHLBI Grant R21HL Hicks was responsible for the conception and design, data analysis, interpretation of the data, and drafting the manuscript. Dan Wang was responsible for acquisition of data, data analysis, and critical revision of the manuscript. Andrea L. Schneider, Michelle C. Johansen, Rebecca F. Gottesman, Kunihiro Matsushita, and Josef Coresh were responsible for interpretation of the data and critical revision of the manuscript. Elizabeth Selvin was responsible for the conception and design, data acquisition, interpretation of the data, and critical revision of the manuscript. All the authors gave final approval of the version of the manuscript to be published. All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author. This article was partially prepared while Dr. Rebecca Gottesman was employed at the Johns Hopkins University School of Medicine. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Dementia and Geriatric Cognitive Disorders. Advanced Search. Skip Nav Destination Close navigation menu Article navigation. Volume 51, Issue 2. Previous Article Next Article. Statement of Ethics. Conflict of Interest Statement. Funding Sources. Author Contributions. Data Availability Statement. Article Navigation. Research Articles March 28 Associations of Peripheral Neuropathy Defined by Monofilament Insensitivity with Mild Cognitive Impairment and Dementia in Older Adults Subject Area: Geriatrics and Gerontology , Neurology and Neuroscience , Psychiatry and Psychology. Hicks a Division of Vascular Surgery and Endovascular Therapy, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. chicks11 jhmi. This Site. Google Scholar. Dan Wang ; Dan Wang. b Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. Schneider ; Andrea L. c Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Michelle C. Johansen ; Michelle C. d Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Rebecca F. Gottesman ; Rebecca F. f National Institute of Neurological Disorders and Stroke Intramural Research Program, Bethesda, Maryland, USA. Kunihiro Matsushita X. Kunihiro Matsushita. Josef Coresh Josef Coresh. Gwen Windham ; B. Gwen Windham. e Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA. Elizabeth Selvin Elizabeth Selvin. Dement Geriatr Cogn Disord 51 2 : — Article history Received:. Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Table 1. View large. View Large. Table 2. Table 3. Table 4. Table 5. The authors have no relevant conflicts of interest to disclose. Epidemiology of peripheral neuropathy and lower extremity disease in diabetes. Search ADS. Prevalence of peripheral neuropathy defined by monofilament insensitivity in middle-aged and older adults in two US cohorts. Sural nerve fibre pathology in diabetic patients with mild neuropathy: relationship to pain, quantitative sensory testing and peripheral nerve electrophysiology. Associations of cardiac, kidney, and diabetes biomarkers with peripheral neuropathy among older adults in the atherosclerosis risk in communities ARIC study. Type 2 diabetes mellitus contributes to cognitive decline in old age: a longitudinal population-based study. Predictors of cognitive decline and mortality of aged people over a year period. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. R D Lawrence Lecture The brain as a target organ in type 2 diabetes: exploring the links with cognitive impairment and dementia. Diabetes, prediabetes, and brain volumes and subclinical cerebrovascular disease on MRI: the atherosclerosis risk in communities neurocognitive study ARIC-NCS. Vascular risk factors and longitudinal changes on brain MRI: the ARIC study. Cerebral MRI findings and cognitive functioning: the atherosclerosis risk in communities study. Neural correlates of domain-specific cognitive decline: the ARIC-NCS study. Centers for Medicare and Medicaid Services. National health and nutrition examination survey — data documentation, codebook, and frequencies: lower extremity disease — peripheral neuropathy LEXPN. Prevalence of lower extremity diseases associated with normal glucose levels, impaired fasting glucose, and diabetes among U. adults aged 40 or older. Demographic and clinical data for the subjects included in the study are shown in Table 1. A total of patients with diabetes, 57 men and 53 women with a mean age of The comparison group consisted of 52 non-diabetic subjects, 20 men and 32 women with No differences were found between patients and non-diabetic controls for age, sex, as well as Beck depression score. The patients had a significant vascular risk factor including hypertension and ischemic heart disease compared with non-diabetic subjects. Table 1 shows the cognitive performance and sexual activity in diabetic patients compared to the comparison group. No differences were observed between the two groups for sexual activity. Since hypertension and ischemic heart disease can be linked to neuropathy and CD, we conducted analysis of covariance ANCOVA to determine the possible confounding effects of hypertension and ischemic heart disease on variables of NCS and MoCA. This analysis demonstrated similar results, even after considering hypertension and ischemic heart disease as confounding factors. According to our results in overall population, there was a significant reverse association between SRAR and severity of NSS and NDS, also a reverse association in each group was observed Table 3. There was no significant association between MoCA and SRAR. Among patients, a weak negative correlation was observed between NDS, NSS, and MoCA score r: We found no statistical differences between NCS parameters and sexual function. Microvascular complications of DM are prevalent despite advances in diabetes prevention and treatment. The present study attempted to identify associations between clinical findings of SD and CD and quantitative aspects of axonal loss in T2DM patients. Our findings showed that diabetic patients have a significantly lower score on MoCA compared with non-diabetic subjects, but we found no correlation between CD based on MoCA score and objective NCS findings. CD in individuals with DM can manifest as MCI and dementia [ 16 ]. A growing body of evidence has linked diabetes with CD [ 16 - 18 ], We expect that DM with PN to be more associated with CD than DM alone. However, the information about the association of PN and CD is different. A retrospective cohort study containing 94 diabetic participants revealed that diabetic people have poorer cognitive performance, but the CD is not correlated with the severity of neuropathy based on NSS and NDS scores [ 19 ]. A recent study demonstrated that although cognitive scores are lower in patients with diabetes, the presence of PN adds no more cognitive decline. The PN is assessed by questionnaire and EDx findings of median, ulnar, and peroneal nerves [ 20 ]. Lin et al in their cross-sectional study of participants using neurofilament examination of both feet, showed that the severity of PN is significantly negatively correlated with cognitive performance [ 21 ]. This result indicates that CD in patients with diabetes may not be limited to microvascular damage of the brain [ 22 ]. In fact, recent data strongly imply that both vascular and neurodegenerative pathologies are associated with cognition in diabetic individuals [ 9 , 23 ]. In the current study, we analyzed the severity of neuropathy using diabetic neuropathy questionnaires as well as quantitative data of NCS together to increase the sensitivity of results. According to previous research sural SNAP amplitude and the SRAR are probably useful parameters for differentiating normal subjects from those with distal polyneuropathy, especially when age adjustment is performed [ 24 , 25 ]. Moreover, we observed a negative correlation between NDS, NSS, and MoCA scores; however, this correlation is weak, which implies increasing in sample size is warranted. Although our findings show diabetic patients do have a worse cognitive function, the control group obtained lower scores as well. Since there was no statistical difference in Beck depression scores between the two groups, this finding may be due to mood disorders or aging effect on cognition [ 26 ]. Also, our results indicate no correlation between NCS parameters and sexual function in DM patients. Prior data showed reverse results based on evaluating neuropathy by physical examination. A recent cross-sectional analysis of 1, men men with diabetes , assessing erectile dysfunction and PN by a single question self-interview and g monofilament testing, respectively, showed decreased lower extremity sensation is a risk factor for erectile dysfunction in both diabetes and non-diabetes people [ 27 ]. A similar study in Japan demonstrated a positive correlation between diabetic neuropathy and severe erectile dysfunction [ 28 ]. Moreover, our different results may be as a consequence of small fiber neuropathy-induced sexual impairment, which preserved large fibers and NCS findings [ 29 ]. We found no differences regarding SD between the two groups. This finding may be a result of a low Beck depression score in all participants, which is in agreement with previous studies [ 30 ]. Our study has several limitations: first, our limited sample size prevented further psychological and neurocognitive evaluations in a different subgroup of DM patients. Future studies should pay particular attention to possible confounding factors such as current life stress and ensure a sufficiently large sample size to take large inter-individual variance into account. Second, although cognitive impairment is not considered a specific feature in patients with DM, a complete neuropsychological assessment is lacking. Third, our hospital is in an area of the city that covers a population with low socio-economic status and lower levels of education, and this might have affected the results of their cognitive performance test. Finally, HbA1C reflects the glycemic status within the last 3 months, to correlate the effect of glycemic control on the NCV findings and overall symptoms in patients with diabetes, we need to conduct a prospective study and check HbA1c in several time points to get a broader view of the glycemic status of the patients. |
| Publication types | Leila Simani a , Muhanna Kazempour b , Mahtab Ramezani c, d , Faezeh Maghsudloo c , Hasan Kazazi e , Sahar Abedi c , Zahra Fatehi e , Fatemeh Ghorbani a , Ehsan Karimialavijeh d, f, g. a Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Science, Tehran, Iran b Department of Rheumatology, Loghman Hakim Hospital, Shahid Beheshti University, Tehran, Iran c Brain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran d Tehran University of Medical Sciences, Tehran, Iran e School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran f Khoula Hospital, Ministry of Health, Muscat, Oman g Corresponding Author: Ehsan Karimialavijeh, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Background: The association between diabetic neuropathy, cognitive impairment, and sexual dysfunction together in patients with diabetes mellites DM is not assessed in prior studies. This study aimed to investigate the association between all these microvascular complications of DM. Methods: A cross-sectional study was conducted on participants diabetic patients and 52 non-diabetic subjects. Neuropathy was evaluated by neuropathy disability score NDS and neuropathy symptom score NSS. Participants underwent cognitive and sexual assessments by Montreal cognitive assessment MoCA , Beck depression score, female sexual function index, and the male sexual function index questionnaires. Results: Both groups showed a decline in cognitive functions; however, diabetic patients had a significantly lower score in MoCA compared to the non-diabetic group mean ± standard deviation: The NCS parameters were notably different in both groups. There were no differences between NCS, NDS, and NSS findings and sexual function. Conclusions: Our data suggest that NCS parameters, even SRAR, do not necessarily correlate with cognitive performance and sexual function. Sexual dysfunction was not correlated with diabetic neuropathy, but clinical findings of NDS and NSS showed a modestly negative correlation with cognitive function. Keywords: Diabetes mellitus; Neuropathy; Sexual dysfunction; Cognition; Nerve conduction study. Diabetes mellitus DM is a common metabolic disorder worldwide and has been rising rapidly, especially in low- and middle-income countries [ 1 ]. 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 ]. All of these can affect the quality of life and impose a considerable social burden. Diabetic sensorimotor polyneuropathy DSPN is the most common type, which can lead to significant disability [ 3 ]. A large number of screening and diagnostic tools are introduced to diagnose DSPN, including electrophysiological studies and standard questionnaires [ 4 ]. The findings of the nerve conduction study NCS provide objective data for confirmation and diagnosis of diabetic neuropathy [ 5 ]. The sexual health of diabetic patients has often been overlooked. Sexual dysfunction SD could be a result of central nervous system dysfunction, autonomic or peripheral nerve damage, psychogenic causes, medications, or a combination of these factors [ 6 ]. SD in male and female patients with DM is reported in various studies [ 6 , 7 ]. In addition, anxiety and depression are prevalent among patients with SD [ 8 ]. Cognitive dysfunction CD is one of the major comorbidities in diabetic patients, which may reflect microvascular brain damage as a consequence of diabetes [ 9 ]. Prior data have shown that multiple cognitive domains including psychomotor speed, memory, executive function, and attention are impaired in T2DM patients [ 11 ]. No study has assessed the association between diabetic neuropathy, cognitive impairment, and SD together. we aimed to investigate the association between electrophysiological findings of neuropathy and CD and SD. In this observational study, patients with diagnosed T2DM, who were referred to our university-affiliated electrodiagnostic EDx laboratory for the investigation of polyneuropathy between September and August , were recruited. All patients above 45 years with a minimum of 5 years of education primary school - secondary school - high school - university were included in this study. Patients with a history of head trauma, cerebral palsy, intellectual disability, dementia or neurodegenerative disease such as epilepsy, multiple sclerosis, and Parkinsonism , malignancy, previously documented psychiatric and sleep disorders, those who had an acute systemic disease endocrine disorder, fluid-electrolyte imbalance, and infection , users of medications neuroleptics, benzodiazepine, and antidepressant that may cause cognitive impairment, severe hearing and visual problems, substance and alcohol users, pregnant women and lactating women were excluded. Non-diabetic individuals matched for age and sex who were referred to the EDx study served as a comparison group. All patients completed a self-administered questionnaire, which addressed diabetes duration, a history of hypertension, ischemic heart disease and medications including neuroleptics, benzodiazepine, and antidepressant. A research nurse calculated the body mass index BMI and blood pressure of participants in a sitting position for 10 min. Peripheral venous blood was sent for routine laboratory tests including hemoglobin A1C HbA1C under fasting conditions. The neuropathy symptom score NSS questionnaire [ 12 ] that is an assessment of four major items that measures the presence, localization, time of appearance, and improvement of neuropathy symptoms, was completed by all participants. The total score ranges from 0 to 10, and the score of 3 - 4, 5 - 6, and 7 - 10 serve as mild, moderate, and severe neuropathy symptoms, respectively. The neuropathy disability score NDS questionnaire was completed by an expert neurologist. The NDS grades neuropathy from 0 no neuropathy to 28 severe neuropathy [ 13 ]. An experienced neurologist performed EDx studies in a quiet room while the participants skin temperature was stabilized to approximately 31 °C. A system from Negar Andishgan Ltd ®. Sensory nerve action potential SNAP was antidromically recorded from bilateral sural and superficial radial nerves. Additionally, compound muscle action potential CMAP was documented from both tibial nerves recording abductor hallucis brevis muscle, and the mean tibial conduction velocity CV , mean tibial distal latency DL and mean amplitude were calculated. The meta-analysis showed that the individuals with T2DM and DPN presented a lower mean cognitive performance than those without DPN Conclusion: The review reveals the great variability in instruments and methodologies, while providing results that support the presence of both global and domain-specific cognitive impairment in diabetic persons with DPN. Keywords: Diabetes mellitus; cognitive function; meta-analysis; peripheral diabetic neuropathy; systematic review. She had sepsis secondary to a gas-producing infection in her plantar left heel four days prior to her presentation. Emergent debridement resulted in a significant deficit to her plantar heel. She achieved wound closure at eight months after her initial presentation and resumed ambulation six weeks after her wound resolved. This particular patient previously struggled with adherence to blood sugar testing, follow-up appointments and non-weightbearing instructions. However, the gravity of her severe foot infection initiated a significant change in her behavior. On her first postoperative day, I formulated a concise, yet specific patient adherence contract to assist her as well as her support system in making positive changes in her behavior. Patient adherence contracts are not financial agreements or substitutes for sturdy medical record documentation. These contracts are solely written commitments from your patients about their intent to adhere to the treatment strategy that will improve their health. Optimum control of these factors can go a long way to reduce the risk of progression of diabetic neuropathy. Canales is Chief of the Division of Podiatry and the Director of the Podiatric Surgical Residency Program at St. Vincent Charity Medical Center in Cleveland. References 1. Is cognitive impairment associated with the presence and severity of peripheral neuropathy in patients with type 2 diabetes mellitus? Diabetol Metab Synd. Curious relationship between cognitive impairment and diabetic retinopathy. J Diabetes Investig. Relationship between type 2 diabetes mellitus and cognitive change in a multiethnic elderly cohort. J Am Geriatr Soc. Change in cognitive function by glucose tolerance status in older adluts: a 4-year prostpective study of the Rancho Bernardo study cohort. Arch Int Med. Cognitive function in an elderly population with persistent impaired glucose tolerance. Diabetes Care. Click here to visit our new Gout Specialty Channel. Sign in. Editorial Information. Editorial Board. Author Guidelines. Organizational Partnerships. Current Issue. Surgical Pearls. Dermatology Diagnosis. |
| Does ‘Cognitive Neuropathy’ Contribute To Non-Adherence In Patients With Diabetes? | Guiding principles for the care of older diabegic with multimorbidity: an approach for clinicians: Alternate-day fasting and weight maintenance Geriatrics Society Expert Panel on iin Cognitive impairment in diabetic neuropathy of Cognitive impairment in diabetic neuropathy Neuropathu with Cogmitive. Cognitive function was assessed using the Test Your Memory TYM instrument, which evaluates 10 cognitive domains: orientation, copying, retrograde and anterograde memory, calculation, verbal fluency, similarities, naming objects, visuospatial ability and executive function. This study showed that NCS measures of nerve fiber functions, even SRAR, do not necessarily correlate with cognitive performance and sexual function. The total score ranges from 0 to 10, and the score of 3 - 4, 5 - 6, and 7 - 10 serve as mild, moderate, and severe neuropathy symptoms, respectively. This association persisted after adjusting for additional risk factors OR 1. |
Cognitive impairment in diabetic neuropathy -
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Citation: Huang W, Lin Z, Sun A, Deng J, Manyande A, Xiang H, Zhao GF and Hong Q The role of gut microbiota in diabetic peripheral neuropathy rats with cognitive dysfunction.
Received: 03 February ; Accepted: 28 March ; Published: 18 April Copyright © Huang, Lin, Sun, Deng, Manyande, Xiang, Zhao and Hong. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY.
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The risk factors for cognitive impairment involve age of onset, and episodes of severe hypoglycemia. It is necessary to conduct clinical studies including all these risk factors to further explore the association between DPN and cognitive dysfunction. 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.
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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.
According to the Cogntiive Cognitive impairment in diabetic neuropathy Mipairment, there are an estimated million people diagnosed with diabetes around the globe. Diabetic neuropathy neuropahy have an dlabetic Cognitive impairment in diabetic neuropathy motor, ij and autonomic nerve fibers in this population. Diabetic neuropathy may affect a Food intolerances in sports of organ systems that set the stage impaimrent amyotrophy, nocturnal diarrhea, gastroparesis, gustatory sweating, cachexia, painful peripheral neuropathy, mononeuropathy, cardiac autonomic neuropathy, postural hypotension, neuropathic bladders and impotence. Less studied is the possible correlation between diabetic neuropathy and cognitive impairment. The aging populace faces a multitude of disease states that deleteriously impact cognitive function. The pathway is not clearly understood but the theory is that poor glycemic control leads to oxidative stress, dyslipidemia and inflammation, which impacts the central nervous system. A study by Moreira and colleagues focused on 94 patients with diabetes 45 of whom had peripheral neuropathycomparing them with 54 patients without diabetes.
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