PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10510679

Motor function in diabetic neuropathy.

H Andersen
View original source ↗Export metadata ↓

Abstract

In contrast to sensory and autonomic disturbances motor function has seldomly been studied in diabetic neuropathy. Recently quantitative studies of long-term type 1 diabetic patients have shown that the strength of the ankle and knee extensors and flexors are moderately impaired. The weakness is closely related to the severity of neuropathy. Applying quantitative electromyography the degree of reinnervation is related to the muscle strength in diabetic patients suggesting the reinnervation to be insufficient. Magnetic resonance imaging of the distal part of the leg has revealed substantial muscular atrophy closely related to the degree of muscle weakness. The present findings indicate that diabetic neuropathy often is a mixed sensory-motor neuropathy.

Explore related subjects

Diabetic NeuropathiesHumansMusclesJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Andersen. 1999. Motor function in diabetic neuropathy.. https://doi.org/10.1111/j.1600-0404.1999.tb00383.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Lamotrigine for treatment of pain associated with diabetic neuropathy: results of two randomized, double-blind, placebo-controlled studies.

To assess the efficacy and tolerability of lamotrigine in pain associated with diabetic neuropathy, two replicate randomized, double-blind, placebo-controlled studies were conducted. Patients (n=360 per study) with painful diabetic neuropathy were randomized to receive lamotrigine 200, 300, or 400 mg daily or placebo during the 19-week treatment phase, including a 7-week dose-escalation phase and a 12-week, fixed-dose maintenance phase. The mean reduction in pain-intensity score from baseline to week 19 (primary endpoint) was greater (p < or = 0.05) in patients receiving lamotrigine 400 mg than placebo in Study 2 (observed scores, -2.7 versus -1.6 on a 0- to 10-point scale). This finding was not replicated in Study 1. Lamotrigine 200 and 300 mg did not significantly differ from placebo at week 19 in either study. Lamotrigine 300 and 400 mg were only occasionally more effective than placebo for secondary efficacy endpoints. The 200-mg dose did not separate from placebo. In a post hoc analysis of pooled data including only patients who reached their target dose, lamotrigine 400 mg conferred greater (p0.05) mean reduction in pain-intensity score from baseline to week 19 than placebo (-2.5 for 300 mg and -2.7 for 400mg versus -2.0 for placebo). Adverse events were reported in 71-82% of lamotrigine-treated patients compared with 63-70% of placebo-treated patients. The most common adverse events with lamotrigine were headache and rash. Compared with placebo, lamotrigine (300 and 400 mg daily) was inconsistently effective for pain associated with diabetic neuropathy but was generally safe and well tolerated.

Diabetic Neuropathies↗
PubMed2006

Intractable epistaxis associated with topiramate administration.

OBJECTIVE: To report a case of a patient who experienced serious, intractable epistaxis warranting emergency department (ED) visits and hospital admission after initiation of topiramate therapy. CASE SUMMARY: A 61-year-old woman with significant cardiovascular disease was started on topiramate 25 mg daily for lower extremity neuropathy. After 7 days of treatment, she began to experience severe, intractable epistaxis that lasted 8 days, warranting an ED visit. The epistaxis resolved 1 week after topiramate discontinuation. Topiramate was restarted 3 months later, and the patient again developed intractable epistaxis. After 2 days of epistaxis, she returned to the ED with significant anginal pain and was admitted to the hospital, where she received 2 units of packed red blood cells. One week after stopping topiramate, the epistaxis stopped. At the time of writing, she had exhibited no epistaxis for 6 months. According to the Naranjo probability scale, topiramate was the probable cause of epistaxis. DISCUSSION: Topiramate is a neuromodulatory compound approved for management of migraines, as well as partial and generalized tonic-clonic seizures. Over the past decade, its use has expanded to include many other neuropathic conditions. Currently, epistaxis has been reported in only 1-4% of patients receiving topiramate in clinical trials; however, these data were derived from a young study population. Like topiramate, calcium-channel blockers (CCBs) modulate voltage-gated L type calcium ion channels. These specific channels are located on vascular smooth muscle and non-contractile tissues such as platelets. Due to their possible antiplatelet effects, CCBs have been associated with an increased risk of hemorrhage, epistaxis, and prolonged bleeding time. The same may hold true for topiramate. CONCLUSIONS: Topiramate, particularly in combination with antiplatelet medications, may be associated with severe, intractable epistaxis. Intractable epistaxis should be added to the list of potentially serious adverse reactions that are monitored when topiramate is administered.

Diabetic Neuropathies↗