Treatment-induced neuropathy of diabetes: challenges in diagnosing neuropathic pain, value of sudomotor function testing.

A patient in his 60s was admitted for an extensive neurological work-up due to progressive asymmetrical, distally pronounced pain in both feet and legs. Conventional pain relievers did not help in pain reduction. A Sudoscan revealed small fibre damage in all extremities indicating an underlying neuropathy. The patient had started insulin treatment around 6 months prior to hospitalisation because of a newly diagnosed late-onset diabetes. Due to a rapid drop in glycated haemoglobin (from over 14% to 6% in 4 months), treatment-induced neuropathy of diabetes (TIND) was hypothesised. On increasing the dose of pregabalin and adding duloxetine, the patient reported improvement of symptoms, which further underlined the suspected diagnosis. Hence, in patients with severe hyperglycaemia, changes in glycaemic control should be stepwise and not rapid; however, to date, no guidelines exist how to avoid TIND.

Predictors of periprocedural brain lesions associated with carotid stenting.

BACKGROUND: Carotid stenting carries a risk of periprocedural stroke. We aimed at determining predictors of cerebral ischemic events associated with stenting for symptomatic carotid stenosis. METHODS: 127 patients who had been studied by diffusion-weighted MR imaging (DWI) before and on the day after carotid stenting were included. Six clinical variables and 5 variables characterizing the target carotid artery and aortic atherosclerosis were analyzed as potential risk factors for new ipsilateral DWI lesions after stenting. RESULTS: Among all variables assessed, only age, length of stenosis and carotid intima-media thickness (IMT) significantly modified the risk of new lesions after stenting. Age ≥68 years, stenosis ≥15 mm and IMT ≥1.3 mm were identified as the best thresholds to predict new lesions. In the subgroup of patients ≥68 years with carotid stenosis ≥15 mm in length and IMT ≥1.3 mm, the risk of new lesions was markedly higher than in patients to whom no more than two of these factors applied (odds ratio 7.250, 95% CI 1.612-34.513, p = 0.005). The use of this simple predictive model correctly identified patients who had new lesions after stenting with high specificity (0.96) and a negative predictive value (0.83), while the positive predictive value was moderate (0.60) and sensitivity was low (0.23). CONCLUSIONS: The risk of stenting for symptomatic carotid stenosis may vary with clinical and morphological patient characteristics. Further research is needed to validate these results and to evaluate the safety of stenting versus endarterectomy in specific patient subgroups.

Carotid plaque surface irregularity predicts cerebral embolism during carotid artery stenting.

BACKGROUND AND PURPOSE: Carotid artery stenting (CAS) is associated with the risk of periprocedural embolic events. The procedural risk may vary with plaque characteristics. We aimed at determining the impact of carotid plaque surface irregularity on the risk of cerebral embolism during CAS. METHODS: Solid microembolic signals (MES) during CAS for symptomatic carotid stenosis were assessed by means of dual-frequency transcranial Doppler ultrasound. Study endpoint was the number of solid MES during CAS in 12 patients with irregular carotid stenosis compared to 12 matched patients with smooth carotid stenosis. RESULTS: A total of 438 solid MES were detected. The cumulative number of solid MES was 329 in patients with irregular plaques and 109 in those with smooth plaques. The proportion of subjects in whom solid MES were detected was higher in the irregular plaque group (11/12) than in the smooth plaque group (5/12) (p = 0.030). The numbers of solid MES per CAS procedure and per hour of CAS procedure were both higher in patients with irregular plaques than in those with smooth plaques (p = 0.008 and 0.015, respectively). CONCLUSIONS: Carotid plaque surface irregularity predicts solid cerebral embolism during stenting of symptomatic carotid artery stenosis.