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The Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS), an assessment tool to determine if pain is predominantly neuropathic, has not been validated in a community setting. Previously identified residents of Olmsted County, Minnesota, with chronic pain were recruited using a stratified randomization process to increase the frequency of neuropathic pain in the study sample. Subjects completed the S-LANSS in mailed and telephone formats, and underwent clinical assessment to determine if a component of their pain was neuropathic. Sensitivity and specificity of the S-LANSS as compared to the clinical assessment were determined. Two hundred and five subjects participated in the study. Eighty-three subjects (40%) had a positive S-LANSS score in the mailed, as did 59 of 173 (34%) in the telephone format, with little inter-subject difference in scores (p=0.57). Clinical assessment identified a component of neuropathic pain in 37% of the sample (75/205). Compared to clinical assessment, sensitivity and specificity in the mailed S-LANSS were 57% (95% CI, 46-69%) and 69% (95% CI, 61-77%), respectively, and in the telephone S-LANSS were 52% (95% CI, 39-64%) and 78% (95% CI, 68-85%), respectively. The sensitivity and specificity of the S-LANSS in both formats were lower than the initial S-LANSS validation study. Differences in survey format and subject population could account for these differences, suggesting that the S-LANSS is best suited as a screening tool and its use to determine the prevalence of neuropathic pain in population studies should be viewed cautiously.

We describe a 61-year-old woman with "broken heart syndrome" (Takotsubo-like cardiomyopathy) after abrupt postsurgical withdrawal of OxyContin. Her medical history was remarkable for long-term opiold dependence associated with the treatment of multi-Joint degenerative osteoarthritis. The patient presented to the emergency department 1 day after discharge from the hospital following total knee arthroplasty revision with acute-onset dyspnea and mild chest pain. She had precordial ST-segment elevation characteristic of acute myocardial infarction and elevated cardiac biomarkers. Emergency coronary angiography revealed no major coronary atherosclerosis. However, the left ventricular ejection fraction was severely decreased (26%), and new regional wall motion abnormalities typical of broken heart syndrome were noted. In addition to resuming her opioid therapy, she was treated supportively with bilevel positive airway pressure, diuretic therapy, morphine, aspirin, metoprolol, enalaprilat, intravenous heparin, nitroglycerin infusion, and dopamine infusion. Ventricular systolic function recovered completely by the fourth hospital day. To our knowledge, broken heart syndrome after opioid withdrawal has not been reported previously in an adult. Our case illustrates the importance of continuing adequate opiate therapy perioperatively in the increasing number of opioid-dependent patients to prevent potentially life-threatening complications such as broken heart syndrome.

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