Be in the Digital Room Where it Happens, Part II: Social Media for Neurology Educators.

Social media has changed the way we communicate and interact. Unsurprisingly, it has also changed how we teach and learn. Younger generations of learners have transitioned from traditional educational sources to digital ones. Medical educators need to adapt to trends in medical education and develop fluency in the digital methods used by medical learners today. This is part two of a two-part series on social media and digital education in neurology. This article provides an overview of how social media can be used as a teaching tool in medical education and provides an overview in which it is grounded. We offer practical strategies on how social media can promote lifelong learning, educator development, educator support, and foster educator identity with accompanying neurology-specific examples. We also review considerations for incorporating social media into teaching and learning practices and future directions for integrating these tools in neurology education.

Be in the Digital Room Where it Happens, Part I: Tweeting & Technology for Career Development.

Social media has become a part of everyday life. It has changed the way we obtain and distribute information, connect, and interact with others. As the number of platforms and users grow, medical professionals have learned the value social media can have in education, research, advocacy, and clinical care initiatives. Platforms provide opportunities to network, build collaborations, and develop a reputation. This is part one of a two-part series. This article provides an overview on how social media can benefit professional career development for clinicians and researchers, as well as for advocacy to raise awareness against biases, disparities, and for patient benefit. We review challenges, limitations, and best practices for social media use by medical professionals with neurology-specific examples.

Focal Electrographic Seizures in a Patient With Autism Spectrum Disorder and Speech Delay.

CASE: A 6-year-old boy with a diagnosis of autism spectrum disorder (ASD) presented to primary care for a new-patient, transfer-of-care evaluation. At the initial encounter, the patient used a maximum of 60 words and was receiving speech and language therapy (SLT) through school. Family history was positive for seizures in the father and paternal grandfather as well as ASD in an older brother. Referrals to genetics, private SLT, and an autism specialist were offered, although the latter was declined by family. The subsequent genetics evaluation resulted in discovery of a small gain on chromosome 1q42.2 and associated partial duplication of the DISC1 gene. The assay could not determine the exact clinical significance of the abnormality, but similarly sized and located abnormalities involving the DISC1 gene are reported in some patients with ASD and developmental delay. During a follow-up pediatrics appointment, the father expressed his wish for further evaluation of causes of autism spectrum disorder (ASD) and requested an electroencephalography (EEG) evaluation. The family concomitantly reported slow improvement in speech with therapy, the use of up to 200 words, and the ability to count to 10. The primary care physician reiterated that EEG and imaging studies are not indicated for an isolated ASD diagnosis with no supporting history or physical examination indications. The clinician discussed ASD-recommended therapies with the family. Neurology referral was made per parental request. The patient subsequently presented to neurology at the age of 7 years. The parents reiterated during the initial neurologic developmental history that the patient had shown some improvement with speech and language therapy in the past 18 months, knew as many as 200 to 300 words, and could put some words together into simple sentences. Gross and fine motor development were felt to be within the normal range for age. The parents also reported some scripting, and mild echolalia was noted on examination. Notably, there was no history of language regression. Apart from language delay, the neurologic examination was otherwise normal at initial evaluation. Given this clinical picture, ASD treatment options were again discussed. Despite education, parents continued to request for EEG evaluation as a workup for the etiology of the patient's ASD. Electroencephalography was ultimately ordered owing to the strong and repeated paternal request despite denial of any seizure-like episodes in the patient. EEG unexpectedly showed extremely frequent, almost constant focal electrographic seizures arising from the T3/T5 electrodes in the speech area of the left temporal lobe, prompting the initiation of oxcarbazepine maintenance therapy. Because of the noted abnormalities on EEG, magnetic resonance imaging (MRI) was obtained. Mild abnormalities were noted on MRI study including possible minimal inferior cerebellar vermian hypoplasia, mildly prominent bodies of the lateral ventricles, and nonspecific, nonenhancing punctate T2 hyperintensities in the subcortical white matter. These findings were not felt to be clinically relevant to the patient's presentation or seizure evaluation. No repeat imaging was ordered. Hindsight is always 20/20. As a clinician evaluating the patient initially, would you have pursued further workup sooner?

Assessment of obstetric brachial plexus injury with preoperative ultrasound.

INTRODUCTION: Tools used in the assessment of obstetric brachial plexus injuries (OBPIs) have traditionally included electrodiagnostic studies, computerized tomography with myelography, and MRI. However, the utility of ultrasound (US) in infants for such assessment has not been extensively examined. METHODS: This retrospective case series reports the preoperative brachial plexus US findings in 8 patients with OBPI and compares US with intraoperative findings. When available, the preoperative US was compared with the preoperative MRI. RESULTS: US revealed abnormalities in all 8 patients. Although MRI detected abnormalities in the majority of patients, US provided accurate information regarding severity and anatomic location of injury in some patients. CONCLUSIONS: US is a relatively inexpensive, noninvasive, painless diagnostic modality that can be used to assess OBPI. This case series suggests that US is a valuable adjunct to current diagnostic modalities. Muscle Nerve 53: 946-950, 2016.

Epileptic spasms: a previously unreported manifestation of WDR45 gene mutation.

WDR45 mutations cause neurodegeneration with brain iron accumulation, usually presenting with early childhood developmental delay and followed by early adulthood extrapyramidal symptoms. Although various seizure types may occur, epileptic spasms have not been reported for this disease. Our patient initially developed a prolonged, focal-onset seizure at three months of age and was subsequently noted to have psychomotor delay. At 11 months of age, she developed epileptic spasms. Her EEG showed hypsarrhythmia. An extensive neurogenetic workup and brain MRI, revealing normal data, ruled out other detectable causes of epileptic spasms. Whole-exome sequencing revealed a de novo, heterozygous deleterious mutation c.400C>T (p.R13X) in WDR45, previously reported to be disease-causing and associated with early childhood global developmental delay and seizures other than epileptic spasms. We conclude that WDR45 mutations should be considered as a possible aetiology in infants with early-onset focal seizures and/or in otherwise undiagnosed cases of epileptic spasms.