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BACKGROUND: The Octave platform is a multifaceted approach to multiple sclerosis (MS) care management that offers a unique, remote, human-tech program that allows persons with MS (PwMS) to record medication administration, symptoms, and communicate with an MS-certified nurse every month between neurology visits. This platform includes a multiprotein serum assay, the Multiple Sclerosis Disease Activity (MSDA) test, quantitative MS-specific MRI reports, and clinical insights (CI). The MSDA panel measures 18 protein biomarkers to attain an MS disease activity score, while CI are extracted from the Octave Care mobile application. OBJECTIVES: Demonstrate the clinical utility of the Octave platform. METHODS: We present a case series of a PwMS enrolled in the prospective, 12-month, randomized wait-list controlled trial MOVING-MS (Measuring Outcomes and Value: an Integrated, Novel solution for Generating insights in MS) who experienced clinically actionable events captured by repeat evaluations with MSDA, MRI, and CI. Quantification of T2 lesion burden and brain volumes on standard-of-care MRIs were evaluated by the platform's algorithm and neuroradiologists. Clinical evaluations taken from the CI mobile application, MS-certified nurse care partner televideo visits, treating neurologist notes, and enhanced MRI reports were compared to MSDA results. RESULTS: In a series of participants with relapsing-remitting MS on disease modifying therapy (DMT), we demonstrate the longitudinal changes in protein biomarker, radiographic, and clinical profiles of the following MS case scenarios: stability, relapse prediction, longitudinal clinical management, and DMT switch. Data captured between visits from the Octave multifaceted platform was enough to determine a clinical action to continue or modify treatment in each case. Furthermore, the MSDA was sensitive to symptom change and treatment within a short time interval. CONCLUSIONS: Clinical utility of the Octave platform in stability, relapse prediction, longitudinal clinical management, and DMT switch was identified in the analysis of individual patient journeys with MS. Comprehensive monitoring of PwMS between standard visits may create opportunities to intervene for better clinical outcomes. Potential health care utilization cost benefits aim to be quantified with future analysis of the MOVING-MS randomized trial with continuous and proactive monitoring of this population.. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endocrine abnormalities associated with myelin oligodendrocyte glycoprotein antibody disease (MOGAD) have not been reported. OBJECTIVES: To review the clinical course in an individual case of MOGAD optic neuropathy with galactorrhea. METHODS: Case report. RESULTS: A 32-year-old right-handed woman (gravida 0 para 0) who was otherwise healthy experienced subacute left eye visual acuity loss associated with painful left eye movements and color desaturation, worsening over 3 to 4 weeks. She had simultaneous transient bilateral galactorrhea with serum prolactin measured at 128.3 µg/L (upper limit of normal, 28.2 µg/L) and subsequent normalization 4 weeks later. Evaluation by endocrinology did not find an alternative cause. She presented to the neuro-ophthalmology clinic 14 months after onset, with findings consistent with a prior optic neuritis. Examination results demonstrated a left-sided relative afferent defect, pinhole-corrected visual acuity of 20/50, and left temporal atrophy. Goldmann perimetry results demonstrated severe left generalized visual field constriction. Optical coherence tomography showed borderline left temporal retinal nerve fiber layer thinning, with normal ganglion cell layers. Autoimmune and rheumatological workup results were negative. Serum myelin oligodendrocyte glycoprotein IgG (MOG-IgG) titer results returned as medium positive at 14 months post symptom onset, with negative aquaporin-4 antibodies. MRI results of brain, orbits, sella, and cervical/thoracic spine with and without gadolinium enhancement were normal. Repeat MOG-IgG titer results 17 months after onset were low positive. As of follow-up at 21 months post onset, she was stable. CONCLUSIONS: To our knowledge, this is the first reported case of a MOGAD-associated optic neuropathy occurring with galactorrhea. [ABSTRACT FROM AUTHOR]

BACKGROUND: There are rare reports of patients with multiple sclerosis (MS) who later develop anti--N-methyl-D-aspartate (NMDA) encephalitis. This overlap is exceedingly rare in adolescents. OBJECTIVES: To discuss a refractory case of MS preceded by anti-NMDA encephalitis in an adolescent. METHODS: Seven years ago, a 14-year-old female adolescent was diagnosed with anti-NMDA encephalitis when she had neuropsychiatric symptoms and results from cerebrospinal fluid (CSF) studies were positive for NMDA receptor antibody. She was treated successfully with cyclophosphamide for a 2-year period. After 3 years, she had the onset of psychiatric symptoms and MRI showed ring-enhancing lesions, with results from CSF studies positive for oligoclonal bands. However, this time she had a negative test result for NMDA antibody in both serum and CSF. RESULTS: She was treated with rituximab every 6 months for 2 years with stable symptoms. After 2 years, she developed left facial weakness and hemibody numbness despite being on rituximab, so she was restarted on cyclophosphamide but had a poor response and required plasmapheresis and additional mycophenolate mofetil. Thereafter, the patient continued on mycophenolate mofetil and a steroid taper. Seven years from initial onset of symptoms, she developed new enhancing lesions consistent with MS and was started on cladribine. Clinically, the patient has been doing well over the last 6 months. CONCLUSIONS: This case highlights the challenges of having an overlap of anti-NMDA encephalitis and MS and the refractory nature of MS to cyclophosphamide and B-cell depletion therapy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is characterized by cerebral vasogenic edema that preferentially affects posterior head regions with accompanying neurologic symptoms. Classic precipitating etiologies of PRES include hypertensive crises, immune therapy, and autoimmune diseases. Neuromyelitis optica spectrum disorder (NMOSD) is an immune-mediated inflammatory disorder targeting aquaporin-4 (AQP4) channels within the central nervous system. NMOSD has 6 core clinical characteristics, including symptomatic brainstem or cerebral syndromes, which can manifest as PRES. However, such syndromes are overlooked given their rarity. To date, only 18 cases of PRES associated with NMOSD have been published. Among these, just 3 cases were identified where PRES appeared as the initial syndrome of NMOSD. OBJECTIVES: To emphasize PRES as an often-overlooked clinical presentation of NMOSD. METHODS: Case report and literature review. RESULTS: A 23-year-old woman with a history of idiopathic thrombocytopenic purpura and systemic lupus presented with headache for 5 days. She was found to have thrombocytopenia (platelet count of 10 x 103/µL) and hypertension (139/91 mm Hg). Clinically, she declined due to posterior fossa vasogenic edema resulting in obstruction of the fourth ventricle and tonsillar herniation. Mannitol administration and surgical intervention were lifesaving, but NMOSD-specific treatments were delayed until AQP4-IgG fluorescence-activated cell sorting titer results returned positive at 1:10,000. CONCLUSIONS: Autoimmune-mediated disruption of AQP4 water channel function predisposes patients to increased cerebral edema. We suspect that NMOSD as etiology of PRES is underrecognized given the co-occurrence of NMOSD with other associated PRES risk factors. Most documented cases, including this report, predominantly involve female patients, who often present with other autoimmune conditions or are receiving treatments associated with PRES. Effective PRES management necessitates addressing its underlying causes, and a delayed NMOSD diagnosis can lead to irreversible neurological harm or death. With the availability of sensitive and specific serum fluorescence-activated cellsorting assays, we recommend broader testing and acknowledgment of NMOSD as a potential underlying cause of PRES. [ABSTRACT FROM AUTHOR]

BACKGROUND: Myelin oligodendrocyte glycoprotein antibody disorder (MOGAD) is an inflammatory demyelinating disease of the central nervous system commonly associated with optic neuritis, myelitis, and acute disseminated encephalomyelitis. Antibodies are formed against MOG, a protein located on the myelin sheath. It can often mimic other autoimmune neuroinflammatory disorders; however, there can be substantial differences in presentation and prognosis. Currently, the gold standard for diagnosis is serum testing for MOG-IgG using cell-based assay (CBA). OBJECTIVES: To describe a case of a patient with recurrent neurological events, negative testing results, and near resolution of his symptoms and lesions without intervention. METHODS: Case review. RESULTS: A 36-year-old right-handed Hispanic man with no past medical history developed left hemisensory loss with no encephalopathy in November 2014. He had received an influenza vaccine 2 weeks prior but had no other recent illnesses. Brain MRI showed right midbrain hyperintensity extending into the right thalamic mesencephalic junction with patchy enhancement and mild edema. Results from serologic tests were unremarkable, and cerebrospinal fluid (CSF) results were noninflammatory. Symptoms resolved without intervention in 4 weeks. Repeat brain MRI in December 2014 showed lesion resolution. In October 2021, he developed right face and tongue numbness, right arm numbness and weakness with slow fine motor movements, dysarthria, and impaired balance. At this time, he had no recent illnesses or vaccines. Brain MRI showed T2 hyperintensity of the left thalamus and midbrain with peripheral enhancement. Spine imaging was unremarkable other than incidentally noted thyroid nodule, of which biopsy results showed atypia of undetermined significance. Vitamin D was low; antinuclear antibodies were 1:40. Findings from other serologic studies for systemic inflammation, MOG, neuromyelitis optica, and infection were unremarkable. Eye examination results were normal. A repeat brain MRI in June 2022 showed resolution of enhancement with subtle T2 hyperintensity in the left dorsolateral thalamus and midbrain. Results from CSF studies were unremarkable. CONCLUSIONS: This is a case of relapsing brainstem syndrome with clinical and radiographic features of MOGAD, suggesting a case of relapsing seronegative MOG antibody disease, as MOG (CBA) testing results were negative. Other potential diagnoses were ruled out. [ABSTRACT FROM AUTHOR]

BACKGROUND: This clinical picture for leucine-rich glioma-inactivated 1 (LGI1) autoimmune encephalitis involves a man in his 60s presenting with faciobrachial dystonic seizures, hyponatremia, and increased T2 medial temporal lobe signal on brain MRI. Proprioceptive-induced reflex seizures are a rare subtype of reflex seizures elicited by active or passive movements of the body or limbs. We describe a patient with several atypical features, including a presentation with proprioceptive stimuli-- induced focal seizures with secondary generalization and focal motor seizure mimicking a neuromuscular disorder, leading to a misdiagnosis of chronic inflammatory demyelinating polyneuropathy and neuromyotonia. OBJECTIVES: Rarely, LGI1 IgG-- positive autoimmune encephalitis can present with proprioceptive-induced reflex seizures that can be triggered by active or passive movements of limbs. METHODS: A man in his late 60s with a history of prostate cancer and borderline diabetes was admitted to the emergency department in late 2019 with 2 consecutive episodes of generalized tonic-clonic seizures. On regaining consciousness, the patient reported a month-long series of episodic right foot cramping and electric shock--like pain. At times, this sensation would spread to his hip, rendering him unable to move the lower half of his body, yet his awareness remained intact. During several instances, the sensation would move farther up, leading to full-body shaking, loss of consciousness, bowel incontinence, tongue biting, and postictal confusion. RESULTS: The patient was admitted to the epilepsy monitoring unit, and his antiepileptic drugs were stopped. A seizure on day 3 of admission started with a tingling/twitching sensation between the big toe and second toe of the right foot. This progressed to a spasm of the right leg, seen as a flexion at the knee and hip, ultimately resulting in bilateral asymmetric tonic seizure followed by generalization of seizure. The patient was able to answer questions until secondary generalization. A second seizure, on day 4 of admission, was similar in progression but started with voluntary flexion at the ankle in the right leg. Both seizures had unclear onset, with the second showing paroxysmal alpha activity in the bifrontal region. The patient's serum workup results revealed positive VGKC-IgG (titer: 515 nmol/L [normal < 0.02 nmol/L]) and LGI1 IgG (cell-based assay; EUROIMMUN). MRI scans revealed right hippocampal atrophy with mild T2 fluid-attenuated inversion recovery changes. After nonresponsiveness to intravenous immune globulin and plasmapheresis, he responded to rituximab. CONCLUSIONS: This case serves as another compelling example of the heterogeneous presentation of LGI1 autoimmune encephalitis, supporting existing data that suggest this condition has diverse manifestations despite some shared symptomatic motifs. A common theme is the rapid improvement in symptoms once an effective treatment is initiated early in the disease course. [ABSTRACT FROM AUTHOR]

BACKGROUND: Multiple sclerosis (MS) is identifiable by the destruction of myelin in the central nervous system leading to gait and balance dysfunction. Our laboratory has shown that backward-walking (BW) velocity in addition to MRI measures may improve fall prediction for people with MS (PwMS). OBJECTIVES: This case series examines the impact of an 8-week BW training program on the superior cerebellar peduncle (SCP) and body of the corpus callosum (CCbody), utilizing myelin water imaging (MWI) and associated changes in gait, postural control, and falls. METHODS: Eight individuals with relapsing-remitting MS and self-reported walking dysfunction on the 12-item Multiple Sclerosis Walking Scale (age range, 51-65 years; Patient Determined Disease Steps score range, 1-5; 2 men, 6 women) participated in this pilot study. Participants completed functional tests (backward- and forward-walking velocity; sway during an eyes-closed, feet-together (ECFT) balance task; postural latency of stepping in reactive balance) and 3T MRI before and after the 8-week intervention, consisting of treadmill and overground BW once per week and home exercises twice per week. Falls were monitored for 6 months after the intervention. The MWI metric of geometric mean of the intra-/extracellular water T2 (geomT2IEW), reflecting axon size/packing density, was estimated from the SCP and CCbody. RESULTS: Of the 8 participants, 7 demonstrated increased geomT2IEW in both the SCP and CCbody, and the change in structure was associated with an improvement in forward-walking (4 of 8 participants) and BW velocity (6 of 8 participants). All participants improved sway metrics during the challenging ECFT task after training. Reactive stepping responses on the push-and-release task improved in 7 participants; 2 participants could not generate reactive steps in the backward direction before training but were able to elicit responses after training. Participants were divided into quartiles by BW speed. Before training, 7 participants fell into the lowest 2 quartiles with velocities of < 0.91 m/s. After training, 4 participants improved their walking enough to move quartiles and reduce their fall risk. CONCLUSIONS: Our results suggest that BW training appears to have both structural (SCP and CCbody) and functional (gait, balance, and reactive stepping) effects over 8 weeks. Future studies should examine structural and functional changes in a larger sample size undergoing more intensive training. Incorporating MWI to assess brain regions potentially associated with BW performance could result in more targeted therapies that enhance clinical outcomes for PwMS. [ABSTRACT FROM AUTHOR]