Amitriptyline relieves diabetic neuropathy pain in patients with normal or depressed mood

Max, Mitchell B.; Culnane, Mary; Schafer, Susan; Gracely, Richard H.; Walther, D. J.; Smoller, Bruce M; Dubner, Ronald

doi:10.1212/wnl.37.4.589

Cited by 641 publications

(220 citation statements)

References 3 publications

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“…One strategy is to use a dose of tricyclic medication too low to achieve a physiological antidepressant effect, and observe whether there is a reduction in depression commensurate with the reduction in pain [38].…”

Section: Discussionmentioning

confidence: 99%

Predictors of depressive symptoms in persons with diabetic peripheral neuropathy: a longitudinal study

et al. 2009

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Aims/hypothesis The aim of the study was to determine whether diabetic peripheral neuropathy (DPN) is a risk factor for depressive symptoms and examine the potential mechanisms for this relationship. Methods This longitudinal study (9 and 18 month followup) of 338 DPN patients (mean age 61 years; 71% male; 73% type 2 diabetes) examined the temporal relationships between DPN severity (mean±SD; neuropathy disability score [NDS], 7.4±2.2; mean vibration perception threshold, 41.5±9.5 V), DPN somatic experiences (symptoms and foot ulceration), DPN psychosocial consequences (restrictions in activities of daily living [ADL] and social selfperception) and the Hospital Anxiety and Depression subscale measuring depressive symptoms (HADS-D; mean 4.9±3.7).Results Controlling for baseline HADS-D and demographic/disease variables, NDS at baseline significantly predicted increased HADS-D over 18 months. This association was mediated by baseline unsteadiness, which was significantly associated with increased HADS-D. Baseline ADL restrictions significantly predicted increased HADS-D and partly mediated the association between baseline unsteadiness and change in HADS-D. Increased pain, unsteadiness and ADL restrictions from baseline to 9 months each significantly predicted increased HADS-D over 18 months. Change in social self-perception from baseline to 9 months significantly predicted increased HADS-D and partly mediated the relationships of change in unsteadiness and ADL restrictions with change in HADS-D. Conclusions/interpretation These results confirm that neuropathy is a risk factor for depressive symptoms because it

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Section: Discussionmentioning

confidence: 99%

Predictors of depressive symptoms in persons with diabetic peripheral neuropathy: a longitudinal study

et al. 2009

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“…Many previous guidelines recommend the medication as a first-line treatment based on few randomized, blinded, placebo-controlled clinical trials that reported significant improvement in neuropathic pain (110,112-116). The effectiveness appeared unrelated to the antidepressant effect (112). A recent Cochrane Review questioned the quality of evidence on amitriptyline by raising concerns for bias given the small sample size in most and concluded that in fact there is no clear evidence for a beneficial effect for amitriptyline on DSPN pain, especially when balanced against spectrum of side effects (117).…”

Section: Monoamine Reuptake Inhibitorsmentioning

confidence: 99%

Diabetic Neuropathy: A Position Statement by the American Diabetes Association

et al. 2016

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“…What is clear is that not all antidepressants have analgesic characteristics and that the analgesic effect is independent of the antidepressant effect. 1,13 Particularly for TCAs, the dose for analgesia is well below therapeutic doses for depression, and the time to analgesic effect is much sooner than for antidepressant activity. It also appears that NE reuptake blockade, not just 5-HT reuptake blockade, is particularly important; hence, TCAs and SNRIs are the most widely used antidepressants for pain control.…”

Section: Antidepressantsmentioning

confidence: 99%