Transverse myelitis (TM) includes a pathobiologically heterogeneous syndrome characterized by acute or subacute spinal cord dysfunction resulting in paresis, a sensory level, and autonomic (bladder, bowel, and sexual) impairment below the level of the lesion. Etiologies for TM can be broadly classified as parainfectious, paraneoplastic, drug/toxin-induced, systemic autoimmune disorders, and acquired demyelinating diseases. We discuss the clinical evaluation, workup, and acute and long-term management of patients with TM. Additionally, we briefly discuss various disease entities that may cause TM and their salient distinguishing features, as well as disorders that may mimic TM.

Objective To assess the ictal symptoms, interictal symptoms, psychiatric comorbidities, and interictal neuro‐otologic examination findings in vestibular migraine (VM). Methods Retrospective chart review of 491 patients seen from August 2014 until March 2018 at a tertiary neurology referral center for vestibular disorders to identify patients fulfilling the 2012 VM criteria. Results One hundred and thirty‐one patients (105 women) were identified. Mean age of VM onset was 44.3 (±13.7) years. Preceding the onset of vestibular symptoms, most had migraine (57.3%) and motion sickness (61.1%). It was common to have a family history of migraine (50.8%) and episodic vestibular symptoms (28.1%). Common ictal symptoms were triggered (visually induced and head‐motion) and spontaneous vertigo, accompanied by photophobia and phonophobia (118/131 [90.1%] patients), nausea (105/131 [80.2%] patients), aural symptoms (79/131 [60.3%] patients), and headache (65/131 [49.6%] patients). Interictally, many experienced visually induced (116/131 [88.6%] patients), head‐motion (86/131 [65.6%] patients), and persistent (67/131 [51.1%] patients) dizziness. Psychiatric comorbidities include anxiety (92/131 [70.2%] patients), depression (53/131 [40.5%] patients), insomnia (38/131 [29.0%] patients), phobic disorders (15/131 [11.5%] patients), and psychogenic disorders (11/131 [8.4%] patients). Common triggers were stress (52/131 [39.7%] patients), bright lights (35/131 [26.7%] patients), weather changes (34/131 [26.0%] patients), and sleep deprivation (34/131 [26.0%] patients). Interictal neuro‐otologic examination was abnormal in 56/131 (42.7%), usually hyperventilation‐induced, head‐shaking‐induced, vibration‐induced, and positional nystagmus. The most common balance‐test finding was impaired sharpened Romberg’s test (22/130 [16.9%] patients). Conclusions In this single center study, we found that VM typically affects women in their 40s, with a personal and family history of migraine. Typical ictal symptoms were triggered and spontaneous vertigo, associated with photophobia and phonophobia, nausea, aural symptoms, and headache. Interictal vestibular symptoms, comorbid psychiatric disorders, and non‐specific interictal neuro‐otologic findings were common.

Dosing intervals up to 8 weeks 5 days did not diminish effectiveness of NTZ therapy. Further monitoring is ongoing to evaluate if the risk of PML is reduced in patients on EID.

In the late 19(th) century, Wilhelm Uhthoff reported on a series of patients with acute optic neuritis who manifested similar recurrent, stereotyped visual symptoms that were of paroxysmal onset, short in duration, and reversible. These 'Uhthoff's phenomena', which are a feature of multiple sclerosis (MS) and other demyelinating diseases, can be triggered by factors including the perimenstrual period, exercise, infection, fever, exposure to high ambient temperatures, and psychological stress. Here, we characterize the clinical, pathophysiological and neurotherapeutic challenges associated with Uhthoff's phenomena, and discuss the differentiation of these events from other paroxysmal, acute or subacute changes in functional capabilities and neurological symptoms in MS. For instance, whereas MS exacerbations are contingent on immune dysregulation, Uhthoff's phenomena are predicated on ion channel modifications, in conjunction with thermoregulatory derangements that transiently alter the conduction properties of demyelinated axons. An understanding of these pathophysiological underpinnings of Uhthoff's phenomena is germane to their recognition and timely treatment.

Our companion paper documents pervasive inhibitory deficits in multiple sclerosis (MS) using ocular motor (OM) measures. Here we investigated the utility of an OM working memory (WMem) task in characterising WMem deficits in these patients as a function of disease status and disease duration. 22 patients with CIS, 22 early clinically definite MS patients (CDMS: <7 years of diagnosis), 22 late CDMS patients (>7 years from diagnosis), and 22 healthy controls participated. All participants completed the ocular motor WMem task, the paced auditory serial addition test (PASAT), and the symbol digit modalities test (SDMT). Clinical disability was characterised in CDMS patients using the Expanded Disability Severity Scale (EDSS). WMem performance was measured as proportion of errors (WMem errors), saccade latency, and relative sensitivity to WMem loading (WMem effect), an indicator of WMem capacity. All patient groups performed more WMem errors than controls with proportion of WMem errors, and degree of WMem effect increasing with increasing disease duration. A larger WMem effect, reflecting poorer WMem capacity, corresponded to poorer performance on neuropsychological measures, and a higher disability score for CDMS patients with the longest disease duration; an observation that suggests wider implication of WMem executive processes with advancing disease. Conspicuously, performance decrements on standard neuropsychological testing did not similarly increase commensurate with disease duration. The ocular motor WMem task appears to meaningfully dissociate WMem deficit from healthy individuals as well as a function of increasing disease duration. Potentially, this task represents a highly informative and objective method by which to ascertain progressive WMem changes from the earliest inception of MS.

The cerebellum guarantees the precision of ocular movements to optimize visual performance and occupies a central role in all classes of eye movements both in real-time control and in long-term calibration and learning (i.e., adaptation).

Background: Vestibular migraine (VM) is the most common neurologic cause of vertigo in adults and results in significant utilization of health care resources, but remains under-recognized and underdiagnosed. Evidence Acquisition: Review of literature in PubMed using the following terms: vestibular migraine, migraine-associated vertigo, vertiginous migraine, benign recurrent vertigo, migraine-associated dizziness, migraine, migraine treatment, Meniere disease (MD), vertebrobasilar ischemia (VBI), posterior circulation stroke, benign paroxysmal positional vertigo, and episodic-ataxia Type 2 (EA2). Results: VM can manifest with a variety of vestibular symptoms, including spontaneous vertigo, triggered vertigo, positional vertigo, and head-motion dizziness. Patients may report more than 1 vestibular symptom. Episodes of vertigo are often, but not always, accompanied by headache. Auditory symptoms are frequently associated with VM attacks and may mimic the manifestations of MD. Other migrainous features that accompany VM attacks include photophobia, phonophobia, osmophobia, and visual aura. Interictally, patients may suffer from persistent dizziness or isolated paroxysmal vestibular symptoms. Mood disorders (particularly anxiety) are often found in VM. Abnormal neuro-otologic findings are not uncommon in patients with VM. Differential diagnoses for VM include MD, VBI, EA2, and migraine with brainstem aura. For rescue treatment, triptans, vestibular suppressants, and/or antiemetic agents may be considered. Pharmacologic migraine preventives (antiepileptics, beta-blockers, and antidepressants) are often useful. Conclusions: The keys to correctly diagnosing VM is identifying a relationship between vestibular symptoms and migrainous features and being aware of the heterogeneity of manifestations of this enigmatic, but treatable, condition. The principles of treatment of VM include rescue therapy, lifestyle modification, nonpharmacologic migraine preventives, pharmacologic migraine prophylaxis, and treatment of comorbidities.

Our ability to control and inhibit behaviours that are inappropriate, unsafe, or no longer required is crucial for functioning successfully in complex environments. Here, we investigated whether a series of ocular motor (OM) inhibition tasks could dissociate deficits in patients with multiple sclerosis (MS), including patients with only a probable diagnosis (clinically isolated syndrome: CIS), from healthy individuals as well as a function of increasing disease duration. 25 patients with CIS, 25 early clinically definite MS patients (CDMS: ≤7 years of diagnosis), 24 late CDMS patients (>7 years from diagnosis), and 25 healthy controls participated. All participants completed a series of classic OM inhibition tasks [antisaccade (AS) task, memory-guided (MG) task, endogenous cue task], and a neuropsychological inhibition task [paced auditory serial addition test (PASAT)]. Clinical disability was characterised in CDMS patients using the Expanded Disability Severity Scale (EDSS). OM (latency and error) and PASAT performance were compared between patient groups and controls, as well as a function of disease duration. For CDMS patients only, results were correlated with EDSS score. All patient groups made more errors than controls on all OM tasks; error rate did not increase with increasing disease duration. In contrast, saccade latency (MG and endogenous cue tasks) was found to worsen with increasing disease duration. PASAT performance did not discriminate patient groups or disease duration. The EDSS did not correlate with any measure. These OM measures appear to dissociate deficit between patients at different disease durations. This suggests their utility as a measure of progression from the earliest inception of the disease.