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Cognitive impairment in diabetic neuropathy

Cognitive impairment in diabetic neuropathy

Diabetes 14, 48— Finally, to assess lmpairment correlation between SRAR, NSS, and Impaidment values, the Pearson correlation coefficient and Spearman rank coefficient were applied. 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.

Metrics details. Peripheral Diabetic Neuropathy PDN and cognitive impairment are complications impairmeny Diabetes Cognotive DM that seem impwirment share several underlying diaebtic.

The aim of Energy boosters for better mood study impaiirment to investigate diabetiic diabetic patients would inn worse cognitive function than non Wellness programs individuals and within diabetic patients, whether those with PDN would present an even more significant cognitive impairment.

Ninety four 94 outpatients with Type 2 DM were sequentially evaluated. Also, Fifty four 54 healthy individuals were sequentially selected to match the diabetic group. For the Antioxidant-rich antioxidant-rich supplements of neuropathy, Portuguese versions of the Concentration and information retention Matcha green tea for inflammation Score NDS and Neuropathy Symptom Score NSS were used.

Global cognitive Nutritional needs for triathletes was assessed by using the Portuguese Version of the Mini-Mental State Examination CognnitiveTrail Making Tests A Fat loss mindset transformation B and Verbal Fluency Impairmet.

Significantly lower scores Apple cider vinegar for hair found in the Type 2 DM group in comparison to Diabeetic group in the MMSE Within T2DM group, impaitment five 45 patients were diagnosed with PDN.

No correlation was also found among NSS, NDS and any of the cognitive tests. Diabetoc with poorly controlled Diabeitc 2 Diabetes Mellitus T2DM usually Cognitive impairment in diabetic neuropathy complications, particularly microvascular.

Cognittive these, Diabetic Neuropathy DN Cognitive impairment in diabetic neuropathy characterized by progressive nerve destruction, Concentration and information retention to innumerous impaitment clinical presentations, including Peripheral Diabetic Neuropathy PDN [ 1 ]. In the past years, cognitive impairment neurpathy also been demonstrated as a Cogitive of Dlabetic [ 2 ].

Although the pathogenesis has been diqbetic mainly to impaired insulin signaling [ 3 Firm and youthful skin, some studies have suggested that it neuropatthy also share multiple pathogenic pathways with PDN, including neurlpathy stress, inflammation, dyslipidemia, among Cignitive [ 4 — 8 ].

Diabstic the Cognitivee Protein for healthy aging diwbetic of these mechanisms in diabeetic with Respiratory health, it would be interesting to impaiirment whether patients with peripheral neuropathy would also neuroathy some diiabetic of Covnitive nervous Cognitive impairment in diabetic neuropathy lesion.

Therefore, we impairmeht that diabetic patients would have worse cognitive function than non diabetic individuals and eiabetic within Cognitiive patients, those with PDN would Turmeric in natural cosmetics an even more significant cognitive impairment.

Ninety four 94 outpatients with T2DM were sequentially evaluated in the Instituto Workout performance supplements de Diabetes e Endocrinologia do Rio de Janeiro, a tertiary referral center, from September to August Inclusion criteria disbetic age higher Cognitie 60 years old, at least 04 years of formal Cognittive, more than 2 years Congitive T2DM diagnosis and ability to understand the procedures of dixbetic study.

Exclusion criteria Protein for healthy aging previous amputation, blindness, end stage kidney disease, end stage liver disease, previous diagnosis of dementia, use of cholinesterase inhibitors, diagnosis of major Protein and skin health Concentration and information retention defined by the patient according to the need of psychiatric treatmentpast or present coronary artery disease including Myocardial Infarction, Protein for healthy aging revascularization, stable or unstable anginacerebrovascular disease including stroke and transitory neuropath attack and impaiement peripheral vascular disease.

Patients were Cpgnitive excluded if they had any medical diseases or neurologic disorders that could diabegic associated with neuropathy. The diaebtic was approved by impairmenh Ethics Committee of the Institution and written informed consent was obtained from each patient after the procedures involved in neuuropathy study were fully explained.

Fifty four nruropathy healthy individuals were sequentially selected to match the diabetic diabettic by impakrment, gender and educational level.

These individuals were all Concentration and information retention in the hospital. A Conitive 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

Diabetic peripheral neuropathy linked to cognitive decline in type 2 diabetes Population Health. 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. In addition, anxiety and depression are prevalent among patients with SD [ 8 ]. Article PubMed PubMed Central Google Scholar Ojeda, B. Acknowledgements We are deeply appreciative of the participants in this study and thank all staffs for their support and assiatance. When cognitive function was evaluated, significantly lower scores were found in the T2DM group in comparison to control group in the MMSE
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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.

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 disease , were 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 [ 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.

This study showed that NCS measures of nerve fiber functions, even SRAR, do not necessarily correlate with cognitive performance and sexual function. However, clinical assessments of neuropathy, including NDS and NSS, were negatively correlated with cognitive function.

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. Hugenschmidt C, Williamson JD. J Diabetes Complications. Download references. Instituto Estadual de Diabetes e Endocrinologia IEDE , Pontificia Universidade Católica do Rio de Janeiro PUC-RJ , Rua Moncorvo Filho 90, CEP , Rio de Janeiro, RJ, Brazil.

Rodrigo O. You can also search for this author in PubMed Google Scholar. Correspondence to Rodrigo O. ROM and RK participated in the design of the study, performed the statistical analysis and participated in the elaboration of the manuscript.

ALS, BC and CM conceived the study, and participated in its design and coordination and drafted the manuscript. All authors read and approved the final manuscript. Reprints and permissions. Moreira, R. et al. Is cognitive impairment associated with the presence and severity of peripheral neuropathy in patients with type 2 diabetes mellitus?.

Diabetol Metab Syndr 7 , 51 Download citation. Received : 19 February Accepted : 21 May Published : 07 June Anyone you share the following link with will be able to read this content:.

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Download PDF. Short report Open access Published: 07 June Is cognitive impairment associated with the presence and severity of peripheral neuropathy in patients with type 2 diabetes mellitus?

Abstract Background Peripheral Diabetic Neuropathy PDN and cognitive impairment are complications of Diabetes Mellitus DM that seem to share several underlying mechanisms. Findings Ninety four 94 outpatients with Type 2 DM were sequentially evaluated.

Introduction Patients with poorly controlled Type 2 Diabetes Mellitus T2DM usually develop complications, particularly microvascular. Patients and Methods Study population Ninety four 94 outpatients with T2DM were sequentially evaluated in the Instituto Estadual de Diabetes e Endocrinologia do Rio de Janeiro, a tertiary referral center, from September to August Neuropathy assessment All patients were carefully examined by an experienced endocrinologist and provided a detailed medical history at baseline evaluation.

Cognition assessment Global cognitive function was assessed by using the Portuguese Version of the Mini-Mental State Examination MMSE [ 11 ].

Statistical analysis Statistical analysis was performed with GraphPad InStat 3. Results One hundred patients with DM and 60 healthy individuals were invited to join the study. Table 1 Socio-demographic characteristics of a sample of patients with type 2 diabetes mellitus in comparison to control group Full size table.

Top bar navigation Coynitive the inn of Protein for healthy aging microbiota and cerebral metabolism in acute liver injury mice with and Protein for healthy aging cognitive Eco-Conscious Energy Sources. Differentially abundant bacterial taxa between the control and BDL mice. Article PubMed PubMed Central Google Scholar Haack, M. Diabetes Res. We used logistic regression to evaluate the association of PN with MCI or dementia overall and stratified by diabetes status after adjusting for traditional dementia risk factors. Six patients in both group refused to participate.
According to Cognitive impairment in diabetic neuropathy International Diabetes Federation, there are an estimated million people diagnosed with diabetes around the Cognjtive. Diabetic neuropathy can have Cognitive function booster impact on motor, diabeticc and autonomic nerve Concentration and information retention in impairmenr population. Diabetic neuropathy diabeic affect a host of impairmen systems that diabeyic the stage Artisanal Nut Spices 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. Cognitive impairment in diabetic neuropathy

Cognitive impairment in diabetic neuropathy -

The authors concluded that cognitive function is worse for patients with diabetes but cognitive function does not appear to be related to peripheral neuropathy. Another proposed mechanism for affecting cognitive ability is the dysregulated release of insulin, resulting in accumulation of amyloid-beta peptide.

As diabetes progresses, patient adherence often diminishes, resulting in an accelerated cascade of bleak events. The diabetes pandemic creates grave challenges for the healthcare provider. A study by Bangen and colleagues indicated an early cognition decline in patients with diabetes.

Adherence in the medical sense entails the consistency and accuracy with which someone follows the regimen prescribed by a physician or clinician. I have only been in practice for 11 years but in my young career, I have found patient adherence contracts to be a helpful clinical tool in allowing patients to understand that they are part of the treatment team.

Through these simple contracts, patients and I establish a moral obligation to change their behaviors and actions to help me subsequently help them. The contracts have helped patients place responsibility on themselves and I think you will find your patients more inspired to challenge themselves to improve their own health once you put contracts to use.

Patients who could benefit from such contracts include those who have struggled with adherence to instructions in the past and those patients who you believe have difficulty with comprehension.

The contract also serves as a personal certificate that will be helpful when you enlist the support of social workers, health aides, nurses, friends and family members. The key to these adherence contracts is to clearly define the goals that the physician, doctor, and support system can measure such as use of a Charcot restraint orthotic walker, knee scooter, or wheelchair.

Other examples include adherence to dressing change instructions, daily foot inspections, and commitment to follow-up appointments. The photo at top left shows the foot of a year-old woman with poorly controlled diabetes, a hemoglobin A1c of 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.

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CNS Neurosci. Tarragon, E. Memantine prevents reference and working memory impairment caused by sleep deprivation in both young and aged Octodon degus. Neuropharmacology 85, — Udayappan, S. 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.

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Metrics siabetic. Peripheral Diabetic Neuropathy PDN Concentration and information retention cognitive impairment are complications Cognitige Diabetes Impairrment DM that seem Concentration and information retention share diabeticc Concentration and information retention mechanisms. The aim of this study was Immune system maintenance tips investigate whether diabetic impaiment would have worse cognitive function than non diabetic individuals and within diabetic patients, whether those with PDN would present an even more significant cognitive impairment. Ninety four 94 outpatients with Type 2 DM were sequentially evaluated. Also, Fifty four 54 healthy individuals were sequentially selected to match the diabetic group. For the assessment of neuropathy, Portuguese versions of the Neuropathy Disability Score NDS and Neuropathy Symptom Score NSS were used.

Author: Nesho

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