Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients

S H Sindrup, B Ejlertsen, H Gjessing, Anders Jørgen Svendsen, A Frøland

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.
OriginalsprogEngelsk
TidsskriftActa Neurologica Scandinavica
Vol/bind79
Udgave nummer5
Sider (fra-til)412-8
Antal sider7
ISSN0001-6314
StatusUdgivet - maj 1989

Fingeraftryk

Peripheral Nerves
Constriction
Hyperglycemia
Insulin
Wrist
Ulnar Nerve
Elbow
Intravenous Infusions

Citer dette

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title = "Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients",
abstract = "The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)",
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Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients. / Sindrup, S H; Ejlertsen, B; Gjessing, H; Svendsen, Anders Jørgen; Frøland, A.

I: Acta Neurologica Scandinavica, Bind 79, Nr. 5, 05.1989, s. 412-8.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients

AU - Sindrup, S H

AU - Ejlertsen, B

AU - Gjessing, H

AU - Svendsen, Anders Jørgen

AU - Frøland, A

PY - 1989/5

Y1 - 1989/5

N2 - The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)

AB - The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)

KW - Adult

KW - Diabetes Mellitus, Type 1

KW - Female

KW - Glucose Clamp Technique

KW - Humans

KW - Hyperglycemia

KW - Male

KW - Middle Aged

KW - Neural Conduction

KW - Peripheral Nerves

KW - Reaction Time

M3 - Journal article

C2 - 2662699

VL - 79

SP - 412

EP - 418

JO - Acta Neurologica Scandinavica

JF - Acta Neurologica Scandinavica

SN - 0001-6314

IS - 5

ER -