Brain Activation and Psychomotor Speed in Middle-Aged Patients with Type 1 Diabetes: Relationships with Hyperglycemia and Brain Small Vessel Disease

Misun Hwang, Dana L. Tudorascu, Karen Nunley, Helmet Karim, Howard J. Aizenstein, Trevor J. Orchard, Caterina Rosano

Research output: Contribution to journalArticle

Abstract

Slower psychomotor speed is very common in patients with type 1 diabetes mellitus (T1D), but the underlying mechanisms are not clear. We propose that hyperglycemia is associated with slower psychomotor speed via disruption of brain activation. Eighty-five adults (48% women, mean age: 49.0 years, mean duration: 40.8) with childhood onset T1D were recruited for this cross-sectional study. Median response time in seconds (longer = worse performance) and brain activation were measured while performing a psychomotor speed task. Exposure to hyperglycemia, measured as glycosylated hemoglobin A1c, was associated with longer response time and with higher activation in the inferior frontal gyrus and primary sensorimotor and dorsal cingulate cortex. Higher activation in inferior frontal gyrus, primary sensorimotor cortex, thalamus, and cuneus was related to longer response times; in contrast, higher activation in the superior parietal lobe was associated with shorter response times. Associations were independent of small vessel disease in the brain or other organs. In this group of middle-aged adults with T1D, the pathway linking chronic hyperglycemia with slower processing speed appears to include increased brain activation, but not small vessel disease. Activation in the superior parietal lobe may compensate for dysregulation in brain activation in the presence of hyperglycemia.

Original languageEnglish (US)
Article number9571464
JournalJournal of Diabetes Research
Volume2016
DOIs
StatePublished - 2016
Externally publishedYes

Fingerprint

Type 1 Diabetes Mellitus
Hyperglycemia
Reaction Time
Parietal Lobe
Brain
Prefrontal Cortex
Occipital Lobe
Gyrus Cinguli
Glycosylated Hemoglobin A
Brain Diseases
Thalamus
Cross-Sectional Studies

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Brain Activation and Psychomotor Speed in Middle-Aged Patients with Type 1 Diabetes : Relationships with Hyperglycemia and Brain Small Vessel Disease. / Hwang, Misun; Tudorascu, Dana L.; Nunley, Karen; Karim, Helmet; Aizenstein, Howard J.; Orchard, Trevor J.; Rosano, Caterina.

In: Journal of Diabetes Research, Vol. 2016, 9571464, 2016.

Research output: Contribution to journalArticle

Hwang, Misun ; Tudorascu, Dana L. ; Nunley, Karen ; Karim, Helmet ; Aizenstein, Howard J. ; Orchard, Trevor J. ; Rosano, Caterina. / Brain Activation and Psychomotor Speed in Middle-Aged Patients with Type 1 Diabetes : Relationships with Hyperglycemia and Brain Small Vessel Disease. In: Journal of Diabetes Research. 2016 ; Vol. 2016.
@article{39d2547ab55441daa3e3064d7c710064,
title = "Brain Activation and Psychomotor Speed in Middle-Aged Patients with Type 1 Diabetes: Relationships with Hyperglycemia and Brain Small Vessel Disease",
abstract = "Slower psychomotor speed is very common in patients with type 1 diabetes mellitus (T1D), but the underlying mechanisms are not clear. We propose that hyperglycemia is associated with slower psychomotor speed via disruption of brain activation. Eighty-five adults (48{\%} women, mean age: 49.0 years, mean duration: 40.8) with childhood onset T1D were recruited for this cross-sectional study. Median response time in seconds (longer = worse performance) and brain activation were measured while performing a psychomotor speed task. Exposure to hyperglycemia, measured as glycosylated hemoglobin A1c, was associated with longer response time and with higher activation in the inferior frontal gyrus and primary sensorimotor and dorsal cingulate cortex. Higher activation in inferior frontal gyrus, primary sensorimotor cortex, thalamus, and cuneus was related to longer response times; in contrast, higher activation in the superior parietal lobe was associated with shorter response times. Associations were independent of small vessel disease in the brain or other organs. In this group of middle-aged adults with T1D, the pathway linking chronic hyperglycemia with slower processing speed appears to include increased brain activation, but not small vessel disease. Activation in the superior parietal lobe may compensate for dysregulation in brain activation in the presence of hyperglycemia.",
author = "Misun Hwang and Tudorascu, {Dana L.} and Karen Nunley and Helmet Karim and Aizenstein, {Howard J.} and Orchard, {Trevor J.} and Caterina Rosano",
year = "2016",
doi = "10.1155/2016/9571464",
language = "English (US)",
volume = "2016",
journal = "Journal of Diabetes Research",
issn = "2314-6745",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Brain Activation and Psychomotor Speed in Middle-Aged Patients with Type 1 Diabetes

T2 - Relationships with Hyperglycemia and Brain Small Vessel Disease

AU - Hwang, Misun

AU - Tudorascu, Dana L.

AU - Nunley, Karen

AU - Karim, Helmet

AU - Aizenstein, Howard J.

AU - Orchard, Trevor J.

AU - Rosano, Caterina

PY - 2016

Y1 - 2016

N2 - Slower psychomotor speed is very common in patients with type 1 diabetes mellitus (T1D), but the underlying mechanisms are not clear. We propose that hyperglycemia is associated with slower psychomotor speed via disruption of brain activation. Eighty-five adults (48% women, mean age: 49.0 years, mean duration: 40.8) with childhood onset T1D were recruited for this cross-sectional study. Median response time in seconds (longer = worse performance) and brain activation were measured while performing a psychomotor speed task. Exposure to hyperglycemia, measured as glycosylated hemoglobin A1c, was associated with longer response time and with higher activation in the inferior frontal gyrus and primary sensorimotor and dorsal cingulate cortex. Higher activation in inferior frontal gyrus, primary sensorimotor cortex, thalamus, and cuneus was related to longer response times; in contrast, higher activation in the superior parietal lobe was associated with shorter response times. Associations were independent of small vessel disease in the brain or other organs. In this group of middle-aged adults with T1D, the pathway linking chronic hyperglycemia with slower processing speed appears to include increased brain activation, but not small vessel disease. Activation in the superior parietal lobe may compensate for dysregulation in brain activation in the presence of hyperglycemia.

AB - Slower psychomotor speed is very common in patients with type 1 diabetes mellitus (T1D), but the underlying mechanisms are not clear. We propose that hyperglycemia is associated with slower psychomotor speed via disruption of brain activation. Eighty-five adults (48% women, mean age: 49.0 years, mean duration: 40.8) with childhood onset T1D were recruited for this cross-sectional study. Median response time in seconds (longer = worse performance) and brain activation were measured while performing a psychomotor speed task. Exposure to hyperglycemia, measured as glycosylated hemoglobin A1c, was associated with longer response time and with higher activation in the inferior frontal gyrus and primary sensorimotor and dorsal cingulate cortex. Higher activation in inferior frontal gyrus, primary sensorimotor cortex, thalamus, and cuneus was related to longer response times; in contrast, higher activation in the superior parietal lobe was associated with shorter response times. Associations were independent of small vessel disease in the brain or other organs. In this group of middle-aged adults with T1D, the pathway linking chronic hyperglycemia with slower processing speed appears to include increased brain activation, but not small vessel disease. Activation in the superior parietal lobe may compensate for dysregulation in brain activation in the presence of hyperglycemia.

UR - http://www.scopus.com/inward/record.url?scp=84960981530&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84960981530&partnerID=8YFLogxK

U2 - 10.1155/2016/9571464

DO - 10.1155/2016/9571464

M3 - Article

C2 - 26998494

AN - SCOPUS:84960981530

VL - 2016

JO - Journal of Diabetes Research

JF - Journal of Diabetes Research

SN - 2314-6745

M1 - 9571464

ER -