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Background: This study was conducted based on a request from the European Medicines Agency to generate robust data on domperidone efficacy in children in the relief of symptoms of nausea and vomiting by assessing the effect of a low-dose and short treatment duration., Methods: In this randomized, double-blind, phase 3 study, children ages 6 months to 12 years with acute gastroenteritis randomly (1:1) received oral domperidone 0.25 mg/kg with oral rehydration therapy (ORT) or matching placebo thrice daily for 2 to 7 days. The proportion of patients with no vomiting episodes (primary endpoint) and patients ages ≥4 years with no nausea episodes (key secondary endpoint) within 48 hours of first treatment administration were evaluated., Results: The study was terminated early following futility analysis. At early termination, 292 patients randomly received domperidone (n = 147) or placebo (n = 145). The proportion of patients with no vomiting episodes within 48-hours of first treatment administration was similar between domperidone (32.0%) and placebo groups (33.8%). Similarly, there was no significant difference in proportion of patients ages ≥4 years with no nausea episodes within 48 hours of first treatment administration between domperidone (35.7%) and placebo (38.6%). Total 13 patients (domperidone, 3.4% [5/147] vs placebo, 5.5% [8/145]) reported ≥1 treatment-emergent adverse events. No deaths or adverse events of special interest (extrapyramidal symptoms and QT prolongation) were reported., Conclusions: Low-dose of domperidone with ORT did not significantly differ from placebo in reducing vomiting and nausea episodes in pediatric patients with acute gastroenteritis (AG), and the safety profile was similar between both groups.

Introduction: Epileptic seizures and epilepsy are part of daily clinical practice in neurology. Yet, the number of false positive diagnoses is surprisingly high. Almost one out of every five patients treated for epilepsy does not really have this diagnosis, which is a high percentage bearing in mind the social and medical consequences that being diagnosed with epilepsy entails., Aims: To summarise the most important diagnostic challenges in epilepsy, to describe possible sources of diagnostic error and to offer advice on how to avoid them., Development: Epilepsy is characterised by a tendency to suffer unprovoked epileptic seizures. The greatest obstacle when it comes to diagnosing a case of epilepsy is the fact that epileptic seizures are transient phenomena that occur relatively infrequently and the physician who must carry out the diagnosis will rarely see them. Moreover, there are other clinical events, such as syncopes or non-epileptic seizures, that may be similar to epileptic seizures in appearance and, consequently, can be mistaken for them. Finally, when interpreting the two most important complementary diagnostic techniques in epileptology, the electroencephalogram and magnetic resonance imaging of the brain, the most common errors must be taken into account in order to prevent mistaken diagnoses., Conclusions: The diagnosis of epilepsy is a challenge and must be based on a detailed and specific medical record. If there are any reasonable doubts, from the outset, about the diagnosis of epilepsy or if the patient does not respond well to the antiepileptic treatment, we recommend referring the patient to a specialised centre to establish a definitive diagnosis.

Objective: Occasionally, diabetic patients develop painless, lower-limb, motor predominant neuropathy. Whether this is a variant of diabetic lumbosacral radiculoplexus neuropathy (DLRPN) (a painful disorder from ischemic injury and microvasculitis), a variant of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) or another disorder is unsettled. Here, we characterize the clinical and pathological features of painless diabetic motor predominant neuropathy., Methods: We identified patients with this syndrome who underwent nerve biopsy. We compared pathological features to 33 DLRPN and 25 CIDP biopsies., Results: 23 patients were identified (22 had type 2 diabetes mellitus); 12 men; median age 62.2 years (range 36-78); median weight loss 30 pounds (range 0-100). Overall, the clinical features were similar to DLRPN except painless patients had more symmetrical and upper limb involvement, with slower progression and more severe impairment. Physiological testing demonstrated pan-modality sensory loss, autonomic abnormalities and axonal polyradiculoneuropathies. Nerve biopsies were similar to DLPRN showing ischemic injury (multifocal fiber loss [11/23], perineural thickening [18/23], injury neuroma [11/23], neovascularization [17/23]) and evidence of altered immunity and microvasculitis (epineurial perivascular inflammation [23/23], prior bleeding [11/23], vessel wall inflammation [15/23], and microvasculitis [3/23]). In contrast, CIDP biopsies did not show ischemic injury or microvasculitis but revealed demyelination and onion-bulbs., Interpretation: 1) Painless diabetic motor neuropathy is painless DLRPN and not CIDP and is caused by ischemic injury and microvasculitis. 2) The clinical features of painless DLRPN are different from typical DLPRN being more insidious and symmetrical with slower evolution. 3) The slower evolution may explain the lack of pain., (Copyright © 2010 American Neurological Association.)

We have examined whether antibodies to myelin-associated glycoprotein (anti-MAG) influence neuropathy occurrence and phenotype in primary (AL IgM) amyloidosis. Anti-MAG and the cross-reacted sulfoglucuronyl paragloboside antibodies (SGPG) were studied in 46 patients with IgM amyloidosis (21 with polyneuropathy), and 21 matched IgM MGUS (monoclonal gammopathies of undetermined significance) controls without neuropathy. We assessed the occurrence, phenotype of neuropathy, and attributes of nerve conduction and their relation to antibody activity. Twenty of 46 patients with IgM amyloidosis (7 with and 13 without polyneuropathy) had elevation of anti-MAG or SGPG by enzyme-linked immunosorbent assay (ELISA). Two of the polyneuropathy patients with IgM amyloidosis had antibodies to MAG based on Western blot (WB) positivity. One of these patients, with the highest anti-MAG titer, had a painful sensory ataxia, with prominent demyelination, and amyloid deposition in sural nerve. The other anti-MAG WB-positive amyloid patient had an axonal neuropathy and dysautonomia. Low levels of anti-MAG antibodies were found in 12 of 21 IgM MGUS controls without neuropathy (mean follow-up, 11 years). We conclude that finding serum anti-MAG antibodies does not exclude the diagnosis of primary amyloidosis. They do not appear to affect the occurrence or expression of polyneuropathy, except possibly in occasional cases with WB positivity.