Point-of-Care Nerve Conduction for the Identification of Neuropathy in Older Adults with Type 1 Diabetes

Introduction: Studies have shown poorer cognitive function in children and adolescents with type 1 diabetes (T1D) as compared to non-diabetic peers. However, little is known about cognitive function in older adults with T1D. Hypothesis: We hypothesized that older adults with T1D and type 2 diabetes (T2D) would have greater cognitive impairment than age, sex, race/ethnicity, and education-matched controls without diabetes. Methods: We compared baseline cognitive impairment among older adults (aged ≥60) from the Study of Longevity in Diabetes (SOLID) with T1D (n=771), T2D (=234) and no diabetes (n=253). Cognitive tests assessed three cognitive domains identified via factor analysis (language, executive function, episodic memory). All cognitive test scores were standardized and cognitive impairment was defined as 1.5 SD below the mean. In logistic regression models adjusted for age, sex, education, and race/ethnicity, we examined the association between diabetes status (T1D, T2D or no diabetes) and cognition on each cognitive domain and on global cognition (average of scores on the 3 domains). Results: In adjusted regression models, compared to older adults without diabetes, those with T1D were more likely to have impaired cognitive function on the language (OR=2.13, 95% CI: 1.08, 4.17) and executive function domains (OR=2.66, 95% CI: 1.36, 5.22). No significant differences in global cognitive impairment or impairment on the episodic memory domain were observed for T1D and no significant differences on any domain were observed for T2D. Conclusions: Our findings suggest that older adults with T1D have greater cognitive impairment than their peers without diabetes; findings were specific to the language and executive function domains, with episodic memory being unaffected. No increase in cognitive impairment was observed for older adults with T2D. Additional research is needed to understand the causes and potentially modifiable factors associated with impaired cognition among older adults with T1D.

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Recurrent diabetic ketoacidosis and cognitive function among older adults with type 1 diabetes: findings from the Study of Longevity in Diabetes

BMJ Open Diabetes Research & Care ◽

10.1136/bmjdrc-2020-001173 ◽

2020 ◽

Vol 8 (1) ◽

pp. e001173 ◽

Cited By ~ 1

Author(s):

Mary E Lacy ◽

Paola Gilsanz ◽

Chloe W Eng ◽

Michal S Beeri ◽

Andrew J Karter ◽

...

Keyword(s):

Older Adults ◽

Type 1 Diabetes ◽

Executive Function ◽

Cognitive Function ◽

Diabetic Ketoacidosis ◽

Brain Health ◽

Psychomotor Speed ◽

Logistic Regression Models ◽

Global Cognitive Function

IntroductionDiabetic ketoacidosis (DKA) is a serious complication of diabetes. DKA is associated with poorer cognition in children with type 1 diabetes (T1D), but whether this is the case in older adults with T1D is unknown. Given the increasing life expectancy in T1D, understanding the role of DKA on brain health in older adults is crucial.Research design and methodsWe examined the association of DKA with cognitive function in 714 older adults with T1D from the Study of Longevity in Diabetes. Participants self-reported lifetime exposure to DKA resulting in hospitalization; DKA was categorized into 0 hospitalization, 1 hospitalization or ≥2 hospitalizations (recurrent DKA). Global and domain-specific cognition (language, executive function/psychomotor speed, episodic memory and simple attention) were assessed. The association of DKA with cognitive function was evaluated via linear and logistic regression models.ResultsTwenty-eight percent of participants (mean age=67 years; mean age at diagnosis=28 years; average duration of diabetes=39 years) reported a lifetime history of DKA resulting in hospitalization (18.5% single DKA; 9.7% recurrent DKA). In fully adjusted models, those with recurrent DKA had lower global cognitive function (β=−0.13; 95% CI −0.22 to 0.02) and lower scores on the executive function/psychomotor speed domain (β=−0.34; 95% CI −0.51 to 0.17). Individuals with recurrent DKA were also more likely to have the lowest level of cognitive function on the executive function/psychomotor speed domain (defined as 1.5 SD below the population mean; OR=3.26, 95% CI 1.43 to 7.42).ConclusionsAmong 714 older adults with T1D, recurrent DKA was associated with lower global cognitive function, lower scores on the executive function/psychomotor speed domain and 3.3 times greater risk of having the lowest level of cognitive function in our sample on the executive function/psychomotor speed domain. These findings suggest that recurrent DKA may negatively impact the brain health of older patients with T1D and highlight the importance of DKA prevention.

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Hypertension Contributes to Neuropathy in Patients With Type 1 Diabetes

American Journal of Hypertension ◽

10.1093/ajh/hpz058 ◽

2019 ◽

Vol 32 (8) ◽

pp. 796-803 ◽

Cited By ~ 8

Author(s):

Georgios Ponirakis ◽

Ioannis N Petropoulos ◽

Uazman Alam ◽

Maryam Ferdousi ◽

Omar Asghar ◽

...

Keyword(s):

Blood Pressure ◽

Type 1 Diabetes ◽

Nerve Conduction ◽

Enzyme Inhibitors ◽

Angiotensin Converting Enzyme Inhibitors ◽

Fiber Density ◽

Converting Enzyme Inhibitors ◽

Perception Threshold ◽

Pressure Lowering

Abstract BACKGROUND Diabetic peripheral neuropathy (DPN) can lead to foot ulceration and amputation. There are currently no disease-modifying therapies for DPN. The aim of this study was to determine if hypertension contributes to DPN in patients with type 1 diabetes mellitus (T1DM). METHODS Subjects with T1DM (n = 70) and controls (n = 78) underwent a comprehensive assessment of DPN. RESULTS Hypertension was present in 40 of 70 T1DM subjects and 20 of 78 controls. Hypertension was associated with abnormal nerve conduction parameters (P = 0.03 to <0.001), increased vibration perception threshold (P = 0.01) and reduced corneal nerve fiber density and length (P = 0.02) in subjects with T1DM. However, after adjusting for confounding factors only tibial compound motor action potential and nerve conduction velocity were associated with hypertension (P = 0.03) and systolic blood pressure (P < 0.01 to <0.0001). Hypertension had no effect on neuropathy in subjects without diabetes. CONCLUSIONS This study shows that hypertension is associated with impaired nerve conduction in T1DM. It supports previous small trials showing that angiotensin-converting enzyme inhibitors improve nerve conduction and advocates the need for larger clinical trials with blood pressure lowering agents in DPN.

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