An Individualized Yoga Intervention for People with Functional Neurological Disorder: Case Series.

Functional neurological disorder (FND) is a heterogeneous condition of neurological symptoms that cannot be linked to a specific neurological cause. Yoga combines movement, breathing, and meditation and has established mind-body effects for people who are managing both psychological and neurological conditions. This case series describes key components of a yoga program for people with FND, evaluating feasibility, acceptability, and efficacy via self-report surveys, clinical assessments, and postintervention interview. Four individuals with FND participated in 45-minute, one-to-one virtual yoga sessions, two times a week for 8 weeks. We measured outcomes in four domains (healthcare utilization, FND symptoms, quality of life and self-efficacy, and function and mobility) at baseline, week 4, and week 8. Assessments included the Psychogenic Movement Disorders Rating Scale, timed up-and-go test, Patient Health Questionnaire-15, Brief Illness Perceptions Questionnaire, 36-Item Short Form Health Survey, and University of Washington Self-Efficacy Scale. Four participants completed at least 8 sessions, and two completed the full intervention (16 sessions). There were no adverse events. Two participants reported positive changes after yoga and improved on all clinical assessments (timed up-and-go test and Psychogenic Movement Disorders Rating Scale). Postintervention interview analysis revealed three themes: negative diagnosis experience, perceived health effects of yoga, and session format preferences. This was an exploratory case series describing a yoga intervention that was associated with some benefits for people with FND (decreased FND symptom severity and increased function, perceived health, quality of life, and self-efficacy). A larger case series is warranted to understand how to best select individuals who would benefit from the program.

COVID-19 manifestations in people with Parkinson's disease: a USA cohort.

BACKGROUND: With the explosion of COVID-19 globally, it was unclear if people with Parkinson's disease (PD) were at increased risk for severe manifestations or negative outcomes. OBJECTIVES: To report on people with PD who had suspected or confirmed COVID-19 to understand how COVID-19 manifested in PD patients. METHODS: We surveyed PD patients who reported COVID-19 to their Movement Disorders specialists at Columbia University Irving Medical Center and respondents from an online survey administered by the Parkinson's Foundation that assessed COVID-19 symptoms, general clinical outcomes and changes in motor and non-motor PD symptoms. RESULTS: Forty-six participants with PD and COVID-19 were enrolled. Similar to the general population, the manifestations of COVID-19 among people with PD were heterogeneous ranging from asymptomatic carriers (1/46) to death (6/46). The most commonly reported COVID-19 symptoms were fever/chills, fatigue, cough, weight loss, and muscle pain. Worsening and new onset of motor and non-motor PD symptoms during COVID-19 illness were also reported, including dyskinesia, rigidity, balance disturbances, anxiety, depression, and insomnia. CONCLUSION: We did not find sufficient evidence that PD is an independent risk factor for severe COVID-19 and death. Larger studies with controls are required to understand this further. Longitudinal follow-up of these participants will allow for observation of possible long-term effects of COVID-19 in PD patients.

An Overview of the Current State and the Future of Ataxia Treatments.

Cerebellar ataxia can be caused by a variety of disorders, including degenerative processes, autoimmune and paraneoplastic illness as well as by gene mutations inherited in autosomal dominant, autosomal recessive, or X-linked fashions. In this review, we highlight the treatments for cerebellar ataxia in a systematic way, to provide guidance for clinicians who treat patients with cerebellar ataxia. In addition, we review therapies currently under development for ataxia, which we feel is currently one of the most exciting fields in neurology.

Stroke Severity Affects Timing: Time From Stroke Code Activation to Initial Imaging is Longer in Patients With Milder Strokes.

Optimizing the time it takes to get a potential stroke patient to imaging is essential in a rapid stroke response. At our hospital, door-to-imaging time is comprised of 2 time periods: the time before a stroke is recognized, followed by the period after the stroke code is called during which the stroke team assesses and brings the patient to the computed tomography scanner. To control for delays due to triage, we isolated the time period after a potential stroke has been recognized, as few studies have examined the biases of stroke code responders. This "code-to-imaging time" (CIT) encompassed the time from stroke code activation to initial imaging, and we hypothesized that perception of stroke severity would affect how quickly stroke code responders act. In consecutively admitted ischemic stroke patients at The Mount Sinai Hospital emergency department, we tested associations between National Institutes of Health Stroke Scale scores (NIHSS), continuously and at different cutoffs, and CIT using spline regression, t tests for univariate analysis, and multivariable linear regression adjusting for age, sex, and race/ethnicity. In our study population, mean CIT was 26 minutes, and mean presentation NIHSS was 8. In univariate and multivariate analyses comparing CIT between mild and severe strokes, stroke scale scores <4 were associated with longer response times. Milder strokes are associated with a longer CIT with a threshold effect at a NIHSS of 4.

Acute Presentation of Nonmotor Symptoms in Parkinson's Disease.

There are a few syndromes involving the nonmotor symptoms of Parkinson's disease and other movement disorders that can quickly lead to severe morbidity and mortality, and, as such, need rapid identification and management. Among these are neuroleptic malignant syndrome, serotonin syndrome, dopamine agonist withdrawal syndrome, and dystonic storm. It is important to maintain a high index of suspicion for these disorders as lack of identification can lead to death. Many of these acutely occurring nonmotor syndromes are primarily the result of imbalances in dopaminergic and serotonergic systems due to changes in pharmacologic management of psychiatric disorders or Parkinson's disease. We discuss these acutely occurring nonmotor symptoms in order to raise awareness and also to highlight how these extremes in symptoms may uniquely shed light on the pathophysiology of Parkinson's disease.

In vivo roles for matrix metalloproteinase-9 in mature hippocampal synaptic physiology and plasticity.

Extracellular proteolysis is an important regulatory nexus for coordinating synaptic functional and structural plasticity, but the identity of such proteases is incompletely understood. Matrix metalloproteinases (MMPs) have well-known, mostly deleterious roles in remodeling after injury or stroke, but their role in nonpathological synaptic plasticity and function in intact adult brains has not been extensively investigated. Here we address the role of MMP-9 in hippocampal synaptic plasticity using both gain- and loss-of-function approaches in urethane-anesthetized adult rats. Acute blockade of MMP-9 proteolytic activity with inhibitors or neutralizing antibodies impairs maintenance, but not induction, of long-term potentiation (LTP) at synapses formed between Schaffer-collaterals and area CA1 dendrites. LTP is associated with significant increases in levels of MMP-9 and proteolytic activity within the potentiated neuropil. By introducing a novel application of gelatin-substrate zymography in vivo, we find that LTP is associated with significantly elevated numbers of gelatinolytic puncta in the potentiated neuropil that codistribute with immunolabeling for MMP-9 and for markers of synapses and dendrites. Such increases in proteolytic activity require NMDA receptor activation. Exposing intact area CA1 neurons to recombinant-active MMP-9 induces a slow synaptic potentiation that mutually occludes, and is occluded by, tetanically evoked potentiation. Taken together, our data reveal novel roles for MMP-mediated proteolysis in regulating nonpathological synaptic function and plasticity in mature hippocampus.