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Bathing epilepsy is a rare form of reflex epilepsy triggered by bathing in room temperature water. It predominates in boys with a mean age of 15 months and its evolution is benign. Diagnosis of bathing epilepsy requires the exclusion of other paroxysmal disorders triggered by water contact. Video‐EEG confirmation of the seizures is necessary to reach a diagnosis of certainty and to allow adequate management. We present the case of a one‐year‐old boy who experienced recurrent episodes of unresponsiveness and cyanosis while bathing in lukewarm water. The diagnosis of bathing epilepsy was confirmed by the video‐EEG recording of a seizure, showing left‐sided frontotemporal delta activity with rapid contralateral spread. Therapy with levetiracetam was effective, subsequently allowing bathing without further seizures.

Interpreting neonatal electroencephalogram (EEG) presents a challenge owing to rapid evolution of EEG patterns occurring during brain maturation in the neonatal period and rich variety of normal patterns of EEG activity, which is difficult to categorize completely. Furthermore, the description of some aspects during maturation varies in different studies. Neonatal EEG is unfamiliar to most neurologists, and its interpretation requires knowledge of the physiological markers of electrogenesis maturation. The purpose of this review was to provide health-care professionals in the neonatal intensive care unit with guidance on the more common normal maturational features of the neonatal EEG. A simplified layout with the essential elements of normal neonatal EEG is included.

A 7-month-old girl developed fever, unconsciousness, and left oral clonic seizures. EEG showed background slowing and periodic lateralized epileptiform discharges (PLED) over right central-temporal regions. Brain MRI revealed a right temporal pole T2 hyperintense lesion (figure 1). CSF PCR was positive for herpes simplex virus 1. Five days after starting treatment with acyclovir (45 mg/kg/day) and phenobarbital (7.5 mg/kg/day), the patient was alert and without seizures, and EEG activity improved. Two weeks later, MRI showed a right temporal-polar malacic area (figure 2), and PCR was negative. Although seen in many diseases,1,2PLED suggest herpes simplex encephalitis in the appropriate clinical context.

We previously developed a collagen tube filled with autologous skin-derived stem cells (SDSCs) for bridging long rat sciatic nerve gaps. Here we present a case report describing a compassionate use of this graft for repairing the polyinjured motor and sensory nerves of the upper arms of a patient. Preclinical assessment was performed with collagen/SDSC implantation in rats after sectioning the sciatic nerve. For the patient, during the 3-year follow-up period, functional recovery of injured median and ulnar nerves was assessed by pinch gauge test and static two-point discrimination and touch test with monofilaments, along with electophysiological and MRI examinations. Preclinical experiments in rats revealed rescue of sciatic nerve and no side effects of patient-derived SDSC transplantation (30 and 180 days of treatment). In the patient treatment, motor and sensory functions of the median nerve demonstrated ongoing recovery postimplantation during the follow-up period. The results indicate that the collagen/SDSC artificial nerve graft could be used for surgical repair of larger defects in major lesions of peripheral nerves, increasing patient quality of life by saving the upper arms from amputation.

We tested whether a preceding muscle contraction changes reciprocal inhibition (RI) between forearm antagonists. RI was studied in 14 healthy subjects by assessing changes in the H reflex (evoked by median‐nerve stimulation) in forearm flexor muscles after conditioning radial‐nerve stimulation at 0‐ and 20‐ms intervals. The maximum sizes of the M wave (Mmax) and H reflex (Hmax) were also measured. After a long‐lasting maximum voluntary handgrip contraction (mean ± SEM: 3.9 ± 0.6 min) of ipsilateral forearm muscles, Mmaxand Hmaxwere unchanged but RI was diminished. After contraction of the contralateral homologous muscles and after contraction elicited by ipsilateral muscle stimulation, RI remained unchanged. These results show that a preceding maximum voluntary contraction (lasting 30 s or more) reduces the activity of the spinal inhibitory interneurons mediating RI. This finding may imply the need to reinterpret results from RI studies in normal subjects and in patients with movement disorders. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1335–1343, 2000.

We tested whether a preceding muscle contraction changes reciprocal inhibition (RI) between forearm antagonists. RI was studied in 14 healthy subjects by assessing changes in the H reflex (evoked by median-nerve stimulation) in forearm flexor muscles after conditioning radial-nerve stimulation at 0- and 20-ms intervals. The maximum sizes of the M wave (Mmax) and H reflex (Hmax) were also measured. After a long-lasting maximum voluntary handgrip contraction (mean ± SEM: 3.9 ± 0.6 min) of ipsilateral forearm muscles, Mmax and Hmax were unchanged but RI was diminished. After contraction of the contralateral homologous muscles and after contraction elicited by ipsilateral muscle stimulation, RI remained unchanged. These results show that a preceding maximum voluntary contraction (lasting 30 s or more) reduces the activity of the spinal inhibitory interneurons mediating RI. This finding may imply the need to reinterpret results from RI studies in normal subjects and in patients with movement disorders. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1335–1343, 2000.

We report a 36-year-old pregnant patient with subtherapeutic trough plasma levels of levetiracetam (LVT) and a breakthrough nocturnal seizure while assuming 3 times a day dosing of the drug. An intensive pharmacokinetic study was performed from immediately before to 11 hours after the morning LVT dose administration and suggested that the patient was not adequately exposed to the drug during the night. After changing the dosing of LVT to 4 times a day, the patient experienced no seizures and delivered a healthy newborn without complications. Afterward, trough plasma levels of LVT remained always within the therapeutic range until delivery, and no major increase of the drug daily dose was required.

Motor conduction block (MCB) has been used as the main diagnostic criterion in multifocal motor neuropathy (MMN). Nonetheless, no agreed definition of block currently exists; the proposed required percent decrement of proximal compound muscle action potential (CMAP) amplitude varies from > 20% to > 50%. The aim of this work was to evaluate, through a follow-up study of patients with MMN, the behaviour of MCB over time. The percent decrement and temporal dispersion of proximal CMAP have also been calculated in normal controls and in patients affected by amyotrophic lateral sclerosis (ALS). The results show that MCB in patients with MMN is a dynamic entity which greatly varies over time and that a > 50% CMAP amplitued reduction may well be preceded by a smaller decrement that is nonetheless indicative of focal myelin damage in the appropriate clinical context. This datum and the results obtained in the control group and in patients with ALS suggest that a reappraisal of the diagnostic criteria for MCB, in cases with clinical and electrophysiological data strongly indicative of MMN, should be considered. Since MMN is a treatable disorder, the use of the proposed less restrictive criteria for the identification of MCB could allow for a promp and more effective treatment.

We report on the case of a 7-year-old boy with Shiga toxin-producing Escherichia coli-related hemolytic uremic syndrome (STEC-HUS), initially presenting with abdominal pain as the only clinical feature and thus requiring differential diagnosis with a surgical emergency. Diagnosis of STEC-HUS was made with the appearance of bloody diarrhea and renal function impairment, and the clinical picture rapidly progressed to multiorgan failure. Relatively late and severe central nervous system (CNS) involvement was present, characterized by subacute encephalitis progressing to coma, which became apparent when the acute phase of thrombotic microangiopathy was resolving. Therefore, neurologic manifestations were thought to be related to reperfusion damage to the CNS and high-dose IV steroid pulse therapy was empirically administered. Following this therapeutic scheme, neurologic involvement resolved with no sequelae. This case offers several points of discussion on the clinical presentation and the diagnostic approach to STEC-HUS, on the related neurologic complications, and on a novel approach to their management.