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We experimentally realize the Peregrine soliton in a highly particle-imbalanced two-component repulsive Bose-Einstein condensate in the immiscible regime. The effective focusing dynamics and resulting modulational instability of the minority component provide the opportunity to dynamically create a Peregrine soliton with the aid of an attractive potential well that seeds the initial dynamics. The Peregrine soliton formation is highly reproducible, and our experiments allow us to separately monitor the minority and majority components, and to compare with the single component dynamics in the absence or presence of the well with varying depths. We showcase the centrality of each of the ingredients leveraged herein. Numerical corroborations and a theoretical basis for our findings are provided through three-dimensional simulations emulating the experimental setting and via a one-dimensional analysis further exploring its evolution dynamics.

Typically, energy levels change without bifurcating in response to a change of a control parameter. Bifurcations can lead to loops or swallowtails in the energy spectrum. The simplest quantum Hamiltonian that supports swallowtails is a nonlinear 2×2 Hamiltonian with nonzero off-diagonal elements and diagonal elements that depend on the population difference of the two states. This work implements such a Hamiltonian experimentally using ultracold atoms in a moving one-dimensional optical lattice. Self-trapping and nonexponential tunneling probabilities, a hallmark signature of band structures that support swallowtails, are observed. The good agreement between theory and experiment validates the optical lattice system as a powerful platform to study, e.g., Josephson junction physics and superfluidity in ring-shaped geometries.

Background and Purpose: Sensory neuronopathy is a cardinal feature of cerebellar ataxia neuropathy vestibular areflexia syndrome (CANVAS). Having observed that two patients with CANVAS had small median and ulnar nerves on ultrasound, we set out to examine this finding systematically in a cohort of patients with CANVAS, and compare them with both healthy controls and a cohort of patients with axonal neuropathy. We have previously reported preliminary findings in seven of these patients with CANVAS and seven healthy controls., Methods: We compared the ultrasound cross-sectional area of median, ulnar, sural and tibial nerves of 14 patients with CANVAS with 14 healthy controls and 14 age- and gender-matched patients with acquired primarily axonal neuropathy. We also compared the individual nerve cross-sectional areas of patients with CANVAS and neuropathy with the reference values of our laboratory control population., Results: The nerve cross-sectional area of patients with CANVAS was smaller than that of both the healthy controls and the neuropathy controls, with highly significant differences at most sites (P < 0.001). Conversely, the nerve cross-sectional areas in the upper limb were larger in neuropathy controls than healthy controls (P < 0.05). On individual analysis, the ultrasound abnormality was sufficiently characteristic to be detected in all but one patient with CANVAS., Discussion: Small nerves in CANVAS probably reflect nerve thinning from loss of axons due to ganglion cell loss. This is distinct from the ultrasound findings in axonal neuropathy, in which nerve size was either normal or enlarged. Our findings indicate a diagnostic role for ultrasound in CANVAS sensory neuronopathy and in differentiating neuronopathy from neuropathy., (© 2018 EAN.)

Objective: The syndrome of cerebellar ataxia with bilateral vestibulopathy was delineated in 2004. Sensory neuropathy was mentioned in 3 of the 4 patients described. We aimed to characterize and estimate the frequency of neuropathy in this condition, and determine its typical MRI features., Methods: Retrospective review of 18 subjects (including 4 from the original description) who met the criteria for bilateral vestibulopathy with cerebellar ataxia., Results: The reported age at onset range was 39-71 years, and symptom duration was 3-38 years. The syndrome was identified in one sibling pair, suggesting that this may be a late-onset recessive disorder, although the other 16 cases were apparently sporadic. All 18 had sensory neuropathy with absent sensory nerve action potentials, although this was not apparent clinically in 2, and the presence of neuropathy was not a selection criterion. In 5, the loss of pinprick sensation was virtually global, mimicking a neuronopathy. However, findings in the other 11 with clinically manifest neuropathy suggested a length-dependent neuropathy. MRI scans showed cerebellar atrophy in 16, involving anterior and dorsal vermis, and hemispheric crus I, while 2 were normal. The inferior vermis and brainstem were spared., Conclusions: Sensory neuropathy is an integral component of this syndrome. It may result in severe sensory loss, which contributes significantly to the disability. The MRI changes are nonspecific, but, coupled with loss of sensory nerve action potentials, may aid diagnosis. We propose a new name for the condition: cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS).

Evidence suggests that patients suffering from Parkinson's Disease (PD) demonstrate less sequence learning in the serial reaction time (SRT) task devised by Nissen and Bullemer (1987). One of the problems with this task is that it is motor intensive and, given the motor difficulties which characterize Parkinson's disease (e.g., tremor, impaired facility of movement, rigidity, and loss of postural reflexes), allows the possibility that patients with PD are capable of sequence learning but are simply unable to demonstrate this through a decrease in reaction time over trials. The present study examined the performance of patients with PD and healthy controls, matched for verbal fluency, on a verbal version of the SRT task where the standard button-pressing response was replaced by a spoken response. Thirteen nondementing patients with PD and 11 healthy controls were administered the SRT task. The PD group demonstrated less sequence learning than the controls and this was independent of age and severity of illness. The results add support to those studies which have found impaired sequence learning using the standard form of the SRT task.

We report on two patients each with tonic, contraversive partial ocular tilt reactions due to unilateral cerebellar lesions: one patient had had a caudal cerebellar hemorrhage, the other a posterior inferior cerebellar artery territory infarct. Both patients had tonic contraversive conjugate ocular torsion; one had skew deviation; neither had a head tilt. One patient had no specific neurologic deficit apart from the conjugate ocular torsion, which was first suspected because of a deviation of the subjective visual horizontal. These observations imply that the ocular tilt reaction (OTR), a brainstem otolith-ocular reflex of probable utricular origin, is under the inhibitory control of the ipsilateral caudal cerebellum, possibly the nodulus, and that a patient with a cerebellar infarct can present with imbalance as the only neurologic symptom and with conjugate ocular torsion as the only specific neurologic sign.

It is accepted that the neck-eye loop (cervico-ocular reflex, COR) is enhanced following loss of vestibular function and that this helps to restore gaze stability during head movements. In this paper we address the question of which structures and/or mechanisms may participate in such plastic enhancement by investigating the COR in 2 patients with absent vestibular function and reduced smooth pursuit-optokinetic eye movements (SP-OKN). The patients had multisystem atrophy involving the vestibular system and the cerebellum. The COR (elicited by angular motion of the trunk relative to the fixed head and angular motion of the head relative to the fixed trunk) was not enhanced in these 2 patients when compared with normal subjects, in contrast to previous findings in a group of patients with absent vestibular function alone. Measurements of slow phase eye movement velocity during SP-OKN stimuli and during combined COR-OKN stimulation (head oscillation relative to the stationary trunk in the light) showed identical values in these two conditions, which indicates that the neck-eye loop did not contribute to gaze stability during head movements. The absence of plastic enhancement of the COR in these patients may be secondary to interruption of SP-OKN pathways at various possible sites and/or to involvement of the vestibulocerebellum, which is known to mediate adaptive plasticity in the vestibulo-ocular reflex.

A light and electron microscopic study was undertaken to determine pathological changes in cutaneous spinal nerves of rabbits following intradermal inoculation with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Infected rabbits were killed at 3, 10, 17, 45 days and 2 years after infection. No abnormalities were seen at 3 days postinoculation. In the nerves of the rabbits killed at 10, 17 and 45 days after infection, axonal (Wallerian-type) degeneration was the main pathological feature. Regeneration, manifested by axonal sprouting, was observed in the nerves of the rabbits killed at 45 days post-inoculation. Neural fibrosis and paucity of unmyelinated axons was the final outcome. The severity of the neural damage not only varied according to the progression of the disease but between nerves taken from the same rabbit. This was probably associated with variation in the numbers of virus particles that had reached the dorsal root ganglion of the dermatome served by a particular nerve. Since alpha HVS (isolate KM 322) provides a model system for the study of virus latency in dorsal root ganglia, and consequently for the study of varicellazoster infection in man, these findings give further insight into the pathology of herpetic neuropathy.

To provide a better insight into the ultrastructural pathology of herpetic neuropathy, quantitative studies were made on cutaneous spinal nerves of normal rabbits and rabbits intradermally infected with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Marked reductions in the numbers and densities of myelinated and unmyelinated axons were found in the nerves of the rabbits killed 17 and 45 days after the infection. Abnormalities in the size distribution of unmyelinated axons were seen at 45 days post-inoculation where axonal sprouting caused a noticeable shift in the fiber population. Two years after virus inoculation reduction in unmyelinated axons and abnormalities in the fiber size distributions characterized by smaller diameters of both myelinated and unmyelinated axons were detected. In these nerves conspicuous fibrosis caused a significant increase in the endoneurial area. At this stage of the infection regenerative changes involving myelinated fibers were found. Since attempts to detect spontaneous reactivation of alpha HVS infection in rabbits have been unsuccessful, the finding of regeneration 2 years after exposure seems in agreement with the view that regenerated myelinated fibers never attain their original size. In the present study although both types of fibers were damaged, morphometric data suggest that unmyelinated axons were more severely affected. Whether this seemingly selective involvement was due to spreading of the virus between axons sharing the same Schwann cell subunit remains to be proved.

In 6 patients anticoagulated with warfarin, nicoumalone, or phenindione the addition of cimetidine prolonged the prothrombin-time (PT) by a mean of 12.6 s (range 5--23 s). In 7 volunteers taking daily subtherapeutic doses of warfarin the addition of cimetidine increased the PT from 19.4 to 22.9 s and the plasma-warfarin concentration from 0.96 to 1.76 microgram/ml. Cimetidine reduced the single-dose clearance of warfarin and antipyrine. The basis of the interaction between cimetidine and oral anticoagulants is probably inhibition of drug metabolism. Care should be exercised in concomitant therapy.

Immunoglobulin preparations from eight patients with clinical features of myasthenia gravis, in whom no serum antibody against acetylcholine receptor (AChR) could be detected, were injected intraperitoneally into mice. Neuromuscular transmission was significantly impaired compared with mice receiving control human immunoglobulin. No antibody bound to the mouse AChR was detected, but there was a small loss (9.4%) of AChR in the mouse diaphragms. Mice injected with myasthenic AChR-antibody-positive immunoglobulin and mice growing hybridoma cells secreting monoclonal AChR antibody showed similar impairment of neuromuscular transmission, but 75% and 94%, respectively, of their muscle AChR had antibody bound and AChR losses were 47% and 60%. The results suggest that a pathogenetic immunoglobulin antibody interferes with neuromuscular transmission in these AChR-antibody-negative patients by binding to non-AChR determinants at the neuromuscular junction. This form of myasthenia is immunologically and physiologically distinct from the AChR-antibody-positive form.

The effects of serum Ig from 7 myasthenia gravis patients on neuromuscular transmission was investigated by passive transfer to mice. A protocol of 60 mg/day for 3 days produced mouse serum levels of anti-mouse AChR that were similar to those in the MG patients, and resulted in corresponding levels (2-76%) of mouse muscle AChR with antibody bound in situ. However, AChR loss was only greater than 20% with one MG preparation. Nevertheless, there was a marked neuromuscular defect in mice injected with 3 preparations which did not necessarily correlate with the degree of AChR loss or the amount of AChRs with antibody bound in situ. We conclude that in some MG patients part of the defect in neuromuscular transmission may result from antibodies binding to other components of the neuromuscular junction.

A patient is presented who has had three six-month episodes of oscillopsia over the last eight years. During the episodes, abnormal smooth pursuit and optokinetic nystagmus were noted, but there were no other abnormalities. Oculography during the most recent episode demonstrated that when tracking from right to left, the patient's smooth pursuit was reversed. There are several features of the case which suggest that the aetiology may be a form of congenital nystagmus. A possible alternative mechanism whereby such an abnormality might arise as an acquired lesion is discussed.

The effect of diflunisal on steady-state warfarin dynamics and kinetics was studied in five healthy men taking daily subtherapeutic doses of warfarin. Diflunisal 500 mg twice daily for 2 wk increased the percentage unbound warfarin from 1.02% to 1.24% and lowered total warfarin from 741 to 533 ng/ml, but did not alter the anticoagulant response (prothrombin complex activity, PCA). When diflunisal was discontinued but warfarin continued, there was a loss of anticoagulant effect and a difference in the rates at which percentage unbound warfarin and total warfarin concentration returned to prediflunisal levels. There was a correlation between plasma diflunisal and percentage unbound warfarin. Diflunisal reduced both the maximum plasma protein-binding capacity for warfarin and the apparent association constant.