Ilaria Iafelice

Ulnar entrapment neuropathy in patients with type 2 diabetes mellitus: an electrodiagnostic study.

AIMS This study aimed to assess the prevalence and electrophysiological features of ulnar entrapment neuropathy in patients with type 2 diabetes mellitus (DM). METHODS Nerve conduction studies (NCS) were performed in a sample of consecutive diabetic patients aged 25-75 years, referred by the Diabetology Unit. NCS of the median, ulnar, radial, peroneal and sural nerves were performed on the non-dominant side. Median entrapment neuropathy at the wrist (MNW) and ulnar neuropathy at the elbow (UNE) and wrist (UNW) were diagnosed according to standard electrodiagnostic criteria. RESULTS Sixty-four patients were enrolled, 28 male (44%), average age 61, average DM duration 14.5 years. Polyneuropathy was diagnosed in 45 subjects (70%). UNE was detected in 22 patients (34%) (4 did not have polyneuropathy), in the abductor digiti minimi in 16, the first interosseus in 14 and in both in 8. UNW was detected in 7 (11%) subjects and MNW in 40 (63%). NCS alterations consistent with ulnar neuropathy were detected in a high proportion of patients (45%), suggesting that the ulnar nerve is very susceptible to focal entrapment in DM. CONCLUSIONS Upper limb sensory and motor NCS, including motor conduction velocity across the elbow, should be considered in the staging of DM patients.

Impact on Prehospital Delay of a Stroke Preparedness Campaign: A SW-RCT (Stepped-Wedge Cluster Randomized Controlled Trial)

Background and Purpose— Public campaigns to increase stroke preparedness have been tested in different contexts, showing contradictory results. We evaluated the effectiveness of a stroke campaign, designed specifically for the Italian population in reducing prehospital delay. Methods— According to an SW-RCT (Stepped-Wedge Cluster Randomized Controlled Trial) design, the campaign was launched in 4 provinces in the northern part of the region Emilia Romagna at 3-month intervals in randomized sequence. The units of analysis were the patients admitted to hospital, with stroke and transient ischemic attack, over a time period of 15 months, beginning 3 months before the intervention was launched in the first province to allow for baseline data collection. The proportion of early arrivals (within 2 hours of symptom onset) was the primary outcome. Thrombolysis rate and some behavioral end points were the secondary outcomes. Data were analyzed using a fixed-effect model, adjusting for cluster and time trends. Results— We enrolled 1622 patients, 912 exposed and 710 nonexposed to the campaign. The proportion of early access was nonsignificantly lower in exposed patients (354 [38.8%] versus 315 [44.4%]; adjusted odds ratio, 0.81; 95% confidence interval, 0.60–1.08; P=0.15). As for secondary end points, an increase was found for stroke recognition, which approximated but did not reach statistical significance (P=0.07). Conclusions— Our campaign was not effective in reducing prehospital delay. Even if some limitations of the intervention, mainly in terms of duration, are taken into account, our study demonstrates that new communication strategies should be tested before large-scale implementation. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT01881152.

Metoclopramide-induced facial and palatopharyngeal myoclonus

A 61-year-old woman developed acute dyslalia, dysphonia, dysphagia, and facial rhythmic jerks 8 hours after the intake of 2 tablets of metoclopramide 10 mg, prescribed for nausea during respiratory infection. Examination revealed dysphonia, dyslalia, dysphagia, and myoclonus in the orbicularis oculi (video 1 on the Neurology® Web site at Neurology.org), orbicularis oris, and palatopharyngeal (video 2); no clicking was audible. Brain MRI, angio-MRI, and EEG were unremarkable. Biperidene 4 mg was given per os: palatopharyngeal myoclonus, dysphonia, and dyslalia improved in 30 minutes and disappeared in 12 hours. Palatal myoclonus may be a rare metoclopramide-induced movement disorder.1,2

“Hummingbird Sign” in Fragile X-Associated Tremor/Ataxia Syndrome

A 64-year-old man progressively developed ataxic gait, 3-Hz high-amplitude, intentional/postural tremor, and dysarthric speech. FMR1 gene analysis revealed a premutation (89 CGG repeats) and a brain MRI showed mesencephalon atrophy with normal pons morphometry (the so-called “hummingbird” or “penguin” sign) along with middle cerebral peduncle hyperintensity, the radiological hallmark of fragile X-associated tremor/ ataxia syndrome (FXTAS). The disease achieved mild severity in 2 years: Neither psychiatric symptoms nor dementia or impairment in daily living activities were reported.

Missing link: Could the elusive Wartenberg's neuritis be a peripheral nerve variant of Fabry's disease?

Sir, Acute sensory multiplex neuropathies are uncommon. Wartenberg was the fi rst to describe in 1958, a small series of patients with ‘migrant sensory neuritis’, consisting of “recurrent, intermittent, remittent neuritis”, with pure sensory involvement both clinically and electrophysiologically.[1] Although evidence of perineuritis has been demonstrated by biopsy of affected cutaneous nerves in a few cases, suggesting an inflammatory -immune origin, the etiology and pathophysiology of Wartenberg’s neuritis (WN) have so far remained elusive,[2] and WN is still a clinical diagnosis.

Parenchyma, Pipes, Perfusion and Penumbra Imaging: The Multimodal CT in Wake-Up Stroke Basilar Thrombosis

logical insights into cerebral hemodynamics. Moreover, it distinguishes infarct core from penumbra, i.e. the volume of tissue contained within the region of mean transit time-cerebral blood volume mismatch, showing which tissue is salvageable by rapid reperfusion. Although, as in this case, the precise time from symptom onset to arrival at hospital is usually unknown/not recorded for most stroke patients (16–28%), who may not be candidates for thrombolysis, recent studies have suggested that the actual onset time of wake-up stroke is close to the wake-up time itself [1] . Furthermore, advanced multimodal acute stroke imaging may identify a subgroup of patients with wake-up/unclear-onset stroke who have a favorable risk-benefit profile for thrombolytic therapy. Indeed, CTP is increasingly available, safe when performed correctly, affordable and usually requires only 5 min more than a standard unenhanced CT [1] , providing an assessment of ischemic tissue viability that transcends from the arbitrary ‘clock time’ . Although stroke imaging has changed remarkably over the past few years and is no longer limited to unenhanced CT, but routinely also includes vascular imaging and tends to integrate perfusion imaging [1, 2] , rarely have full findings of multimodal CT imaging in wake-up stroke basilar thrombosis been reported. Herein we report the CT angiography (CTA) findings ( fig. 1 a, b; online suppl. video 1; for all online suppl. material, see www.karger.com/doi/10.1159/000355469), showing a wake-up stroke basilar thrombosis in a 44-yearold woman who was found unarousable. Although the time of onset of the stroke was unknown, CT perfusion (CTP) documented a large area of hypoperfusion in the pons and both cerebellar hemispheres with perfusion mismatch data consistent with wide, favorable ischemic penumbra ( fig. 1 c, d). Intra-arterial thrombolysis was performed with basilar artery recanalization ( fig. 1 e, f; online suppl. video 2); the follow-up showed a small ischemic area on the pons and normal neurological status. Nowadays, CTP expands the role of CT in the evaluation of acute stroke patients by providing pathophysioReceived: July 2, 2013 Accepted: September 1, 2013 Published online: January 7, 2014