Anterior tarsal tunnel syndrome: a misunderstood and a misleading entrapment neuropathy.

Anterior tarsal tunnel syndrome (ATTS) is a rare entrapment neuropathy of the deep peroneal nerve beneath the extensor retinaculum on the top of the ankle. ATTS is often asymptomatic or olygosymptomatic. There are few reports describing the ATTS. We describe the clinical and electrophysiological features of 85 patients with unilateral or bilateral ATTS prospectively collected between January 2000 and December 2010 in our laboratory of Clinical Neurophysiology. This entrapment neuropathy remains poorly diagnosed and it might be misleading when performing a diagnostic EMG-ENG examination for suspected polyneuropathy or lumbosacral radiculopathy.

Oxidative stress in ischaemic stroke.

BACKGROUND: Production of reactive oxygen species after ischaemic stroke may enhance tissue damage through multiple molecular pathways. MATERIALS AND METHODS: In this study, we examined the serum levels of lipoperoxide and hydroperoxide, conjugated dienes and total antioxidant capacity levels in 50 patients with acute ischaemic stroke (T0) to evaluate the possibility to use them as specific biochemical markers for cerebral ischaemia. Determinations were repeated after a month (T1) to correlate their relative changes with clinical evolution. RESULTS: Lipoperoxide, hydroperoxide and conjugated diene levels in platelets were significantly higher in the early stages with respect to their late evaluation. On the contrary, total antioxidant capacity showed a significant increase at T1 with respect to T0. A significant negative correlation between total antioxidant capacity and NIHSS score at T0 and T1 was found. There was a significant positive correlation between lipoperoxide, hydroperoxide and conjugated dienes levels and NIHSS score at T0 and at T1. CONCLUSIONS: These findings suggest that changes in free radical generation and consequent oxidative stress may have a role in the pathogenesis of acute ischaemic lesions. The activation of defence mechanisms like total antioxidant capacity could be involved in the limitation of ischaemic damage progression.

Severe carotid stenosis and impaired cerebral hemodynamics can influence cognitive deterioration.

OBJECTIVE: To evaluate whether severe carotid stenosis and related hemodynamics impairment may increase the risk of cognitive deterioration in asymptomatic subjects. METHODS: A total of 210 subjects with unilateral asymptomatic severe carotid stenosis and 109 healthy controls were included and prospectively evaluated for a 36-month period. At entry, demographics, vascular risk profile, and pharmacologic treatments were defined. Cerebral hemodynamics was assessed by transcranial Doppler-based breath-holding index (BHI) test. Cognitive status was evaluated with the Mini-Mental State Examination (MMSE) at entry and at the end of the follow-up period. Cognitive deterioration was defined as a decrease in the MMSE score of 3 points or more during the overall follow-up period. RESULTS: Subjects with carotid stenosis showed an increased probability of developing cognitive deterioration compared with the group without stenosis (odds ratio [OR] 4.16 [95% confidence interval (CI) 1.89-9.11]; p < 0.001). The presence of an impaired BHI ipsilateral to the stenosis was associated with an increased incidence of reduction in cognitive performance (OR 14.66 [95% CI 7.51-28.59]; p < 0.001). CONCLUSIONS: Our findings show that the presence of a severe carotid stenosis influences cognitive deterioration over a 36-month period in asymptomatic subjects. An associated hemodynamic impairment significantly increases the risk. Evaluation of functional consequences of carotid stenosis may offer the opportunity to select a group with an increased risk of developing cognitive impairment from subjects with asymptomatic severe carotid stenosis.