Brainstem Infarction and Panuveitis due to Sarcoidosis Successfully Treated with Steroid Pulse Therapy

A 36-year-old man visited our hospital because of blurred vision and redness of the conjunctiva. Slit-lamp examination showed panuveitis. Two days later, he suddenly experienced dizziness, speech disturbance, paralysis of his right extremities, and gait disturbances. Neurological examinations suggested that his symptoms were caused by a left lateral medullary lesion. He also had erythema mainly on his trunk. Magnetic resonance imaging (MRI) of his brain demonstrated a small infarct on the left side of the medulla oblongata. Clinical presentation and MRI findings were consistent with the diagnosis of a Wallenberg's syndrome. He also had bilateral hilar lymphadenopathy. A skin biopsy showed granulomatous nodular dermatitis compatible with sarcoidosis. He was treated with steroid pulse therapy and his neurological and ocular symptoms immediately improved. Only seven similar cases of intracranical sarcoidosis have been reported, but none had been treated with steroid pulse therapy. We recommend that steroid pulse therapy be considered to treat patients with sarcoidosis with signs of lesions in the central nervous system

A chin cap type protractor device was used for skeletal mandibular protrusion,A case of orthodontic treatment by extracting maxillary and maxillary premolars while paying attention to lateral changes

Summary This case was a 10–years and 10–month–old girl who visited the hospital with a complaint of opposite anterior bite. Facial findings showed no anterior asymmetry, but lateral features showed a concave type. The molar relationship was Angle Class III on both sides,and the left side showed a more prominent class III relationship. Anterior cross bite and labial inclination of both upper and lower side anterior teeth were observed. The diagnosis was a case of skeletal mandibular protrusion with functional factors. It was decided to use a chin–cap type anterior traction device of the upper jaw that can promote the growth of the upper jaw and suppress the growth of the lower jaw. In the phase of adult treatment, it was decided to extract the maxillary right first premolar, the maxillary left second premolar,and the mandibular bilateral first premolar to establish Angle Class I. At the end of the dynamic treatment, the molar relationship showed Angle Class I on both the left and right sides, and a tight and stable cusp fitting was maintained. Although ANB did not change on the lateral cephalogram, labial inclination was observed on both upper and lower anterior teeth. The dynamic treatment period was 2 years and 11 months, and the end age was 18 years and 1 month. No problem was observed in the occlusal state 4 years after the device was removed, but it will be carefully observed in the future

A favorable outcome of intensive immunotherapies for new-onset refractory status epilepticus (NORSE)

Abstract Background New-onset refractory status epilepticus (NORSE) is a newly defined critical disease entity characterized by prolonged periods of refractory epileptic seizure with no readily identifiable cause in otherwise healthy individuals. Its etiology is uncertain, but autoimmune encephalitis is a possible candidate for the underlying cause of this condition. Immunotherapies could be considered for this condition, but its efficacy is not established. Case presentation A 31-year-old man with no prior history presented with refractory status epilepticus. His seizure persisted even with multiple anti-epileptic drugs and required prolonged general anesthesia under mechanical ventilation. Magnetic resonance imaging and cerebrospinal fluid did not indicate the cause of seizure, and autoantibodies related to encephalitis were not detected. It was speculated that the patient had occult autoimmune encephalopathy because of its acute-onset clinical course preceded by fever, even without definite evidence of an autoimmune mechanism. The patient received intravenous methylprednisolone, plasma exchange, and intravenous immunoglobulin in succession and manifested a favorable outcome after these treatments. Conclusion Our case supports the efficacy of immunotherapies for NORSE even though it does not manifest definite evidence for autoimmune background. Clinicians should consider these immunotherapies for NORSE as early as possible, because this condition is associated with high mortality and morbidity owing to prolonged seizure activity and long-term intensive care including general anesthesia and mechanical ventilation

Augmenting LTP-like plasticity in human motor cortex by spaced paired associative stimulation

Paired associative stimulation (PASLTP) of the human primary motor cortex (M1) can induce LTP-like plasticity by increasing corticospinal excitability beyond the stimulation period. Previous studies showed that two consecutive PASLTP protocols interact by homeostatic metaplasticity, but animal experiments provided evidence that LTP can be augmented by repeated stimulation protocols spaced by ~30min. Here we tested in twelve healthy selected PASLTP responders the possibility that LTP-like plasticity can be augmented in the human M1 by systematically varying the interval between two consecutive PASLTP protocols. The first PASLTP protocol (PAS1) induced strong LTP-like plasticity lasting for 30-60min. The effect of a second identical PASLTP protocol (PAS2) critically depended on the time between PAS1 and PAS2. At 10min, PAS2 prolonged the PAS1-induced LTP-like plasticity. At 30min, PAS2 augmented the LTP-like plasticity induced by PAS1, by increasing both magnitude and duration. At 60min and 180min, PAS2 had no effect on corticospinal excitability. The cumulative LTP-like plasticity after PAS1 and PAS2 at 30min exceeded significantly the effect of PAS1 alone, and the cumulative PAS1 and PAS2 effects at 60min and 180min. In summary, consecutive PASLTP protocols interact in human M1 in a time-dependent manner. If spaced by 30min, two consecutive PASLTP sessions can augment LTP-like plasticity in human M1. Findings may inspire further research on optimized therapeutic applications of non-invasive brain stimulation in neurological and psychiatric diseases

Computational modeling of the time course of PAS₁ and PAS₂ effects.

<p>MEP amplitudes as a function of time modeled from the experimental MEP raw data independently for PAS₁ and PAS₂ at all IPIs. PAS₁ and PAS₂ model functions, i.e. the time course of MEP amplitude changes after PAS₁ vs. those after PAS₂, were significantly different at all IPIs (<i>P</i> < 0.0001 each). In addition, PAS₂ effects at IPI₁₀ and IPI₃₀ were significantly different from PAS₂ effects at IPI₆₀ and IPI₁₈₀ (<i>P</i> < 0.0001), and PAS₂ effects at IPI₁₀ from PAS₂ effects at IPI₃₀ (<i>P</i> = 0.033), but not PAS₂ effects at IPI₆₀ from those at IPI₁₈₀ (<i>P</i> > 0.5). Experimental data are shown as mean ± SEM. Note that data for PAS₂ at time points 60min and 180min post PAS₂ are from six subjects only, whereas all other data are from twelve subjects (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0131020#sec002" target="_blank">Material and Methods</a>). Y-axis, logarithmic scaling.</p

PAS₂-induced increase in MEP amplitude after PAS₁-priming in the control experiment (IPI_30adj).

<p>MEP amplitudes at time point B2 immediately before PAS₂ were successfully readjusted by reducing the stimulation intensity (SI'_1mV) to match baseline MEPs at time point B0 (PAS₁, MEP_B2/B0). Despite this readjustment, PAS₂ induced a similar increase in MEP amplitudes in the control (IPI_30adj) compared to the main experiment (IPI₃₀) (PAS₂, MEP_Pmean/MEP_B2). *, <i>P</i> < 0.05, one-sample two-tailed <i>t</i> tests; #, <i>P</i> < 0.01, unpaired two-tailed <i>t</i> test. Data from the control experiment are from nine subjects, means ± 1 SEM.</p

PAS₁-induced increases in MEP amplitude.

<p>PAS₁ resulted in comparable immediate MEP amplitude increases (MEP_B1/MEP_B0) in all IPI conditions (data not shown). At time point B2 (MEP_B2/MEP_B0), MEP amplitude increases were present 10min (IPI₁₀) and 30min (IPI₃₀) after PAS₁, but no longer at 60min (IPI₆₀) and 180min (IPI₁₈₀) after PAS₁. Asterisks indicate significant differences from 1 (<i>P</i> < 0.01; one-sample two-tailed <i>t</i> tests). Note that MEP_B2/MEP_B0 was not significantly different between conditions IPI₁₀ and IPI₃₀ (<i>P</i> > 0.09; paired two-tailed <i>t</i> tests). Data are means ± 1 SEM from twelve subjects.</p